# 5 Surgical infection

# ANTIMICROBIAL TREATMENT OF SURGICAL INFECTION Prin

ANTIMICROBIAL TREATMENT OF SURGICAL INFECTION Principles

Antimicrobials may be used to prevent or treat established surgical infection. The use of  antibiotics for the treatment of  established surgi - cal infection ideally requires recognition and determination of the sensitivities of  the causative organisms. Antibiotic therapy Figure 5.18 

Infected animal bite/wound of the upper thigh, treated
by open therapy following virulent staphylococcal infection.

empirical and later modified depending on microbiological findings on culture and sensitivity . Once antibiotics have been administered, it may not be possible to grow bacteria from the wound and so the opportunity to ascertain the most appropri ate antibiotic sensitivities is lost if  a patient’s condition does not improve on empirical antibiotic therapy . Antibiotics alone are rarely su ffi cient to treat SSIs, which may also need open drainage and debridement ( Summary box 5.14 ). Summary box 5.14 Principles for the use of antibiotic therapy /uni25CF /uni25CF /uni25CF There are two approaches to antibiotic treatment: A narrow-spectrum antibiotic may be used to treat a known sensitive infection; for example, MRSA (which may be isolated from pus) is usually sensitive to vancomycin or teico planin, but not flucloxacillin. Combinations of broad-spectrum antibiotics can be used when the organism is not known or when it is suspected that several bacteria, acting in synergy , may be responsible for the infection. For example, during and follow ing emergency surgery requiring the opening of  perforated or ischaemic bowel, any of the gut organisms may be responsi b le for subsequent peritoneal or bacteraemic infection. In this case, a broad-spectrum antibiotic such as teicoplanin or mero penem, which are e ff ective against a wide range of  aerobic bacteria, is combined with metronidazole, which is e ff ectiv against anaerobic bacteria. Alternatively , triple therap y is used with amoxicillin, gentamicin and metronidazole. The use of such broad-spectrum antibiotic strategies should be guided by specialist microbiological advice. If  clinical response is poor after 3–4 days, there should be a re-evaluation with a review of  available culture and sensitivity results and further investi gations requested to exclude the development or persistence of infection such as a collection of  pus. In surgical units in which resistant Pseudomonas or other Gram-negative species (such as Klebsiella ) have become ‘resident opportunists’, it may be necessary to rotate anti pseudomonal and anti-Gram-negative antibiotic therapy ( Summary box 5.15 ). Summary box 5.15 Treatment of commensals that have become opportun ist pathogens /uni25CF /uni25CF 

Antibiotics do not replace surgical drainage of infection
Only spreading infections or signs of systemic infection justify
the use of antibiotics
Whenever possible, the organism and sensitivity should be
determined
They are likely to have multiple antibiotic resistance
It may be necessary to rotate antibiotics

ANTIMICROBIAL TREATMENT OF SURGICAL INFECTION Principles

Antimicrobials may be used to prevent or treat established surgical infection. The use of  antibiotics for the treatment of  established surgi - cal infection ideally requires recognition and determination of the sensitivities of  the causative organisms. Antibiotic therapy Figure 5.18 

Infected animal bite/wound of the upper thigh, treated
by open therapy following virulent staphylococcal infection.

empirical and later modified depending on microbiological findings on culture and sensitivity . Once antibiotics have been administered, it may not be possible to grow bacteria from the wound and so the opportunity to ascertain the most appropri ate antibiotic sensitivities is lost if  a patient’s condition does not improve on empirical antibiotic therapy . Antibiotics alone are rarely su ffi cient to treat SSIs, which may also need open drainage and debridement ( Summary box 5.14 ). Summary box 5.14 Principles for the use of antibiotic therapy /uni25CF /uni25CF /uni25CF There are two approaches to antibiotic treatment: A narrow-spectrum antibiotic may be used to treat a known sensitive infection; for example, MRSA (which may be isolated from pus) is usually sensitive to vancomycin or teico planin, but not flucloxacillin. Combinations of broad-spectrum antibiotics can be used when the organism is not known or when it is suspected that several bacteria, acting in synergy , may be responsible for the infection. For example, during and follow ing emergency surgery requiring the opening of  perforated or ischaemic bowel, any of the gut organisms may be responsi b le for subsequent peritoneal or bacteraemic infection. In this case, a broad-spectrum antibiotic such as teicoplanin or mero penem, which are e ff ective against a wide range of  aerobic bacteria, is combined with metronidazole, which is e ff ectiv against anaerobic bacteria. Alternatively , triple therap y is used with amoxicillin, gentamicin and metronidazole. The use of such broad-spectrum antibiotic strategies should be guided by specialist microbiological advice. If  clinical response is poor after 3–4 days, there should be a re-evaluation with a review of  available culture and sensitivity results and further investi gations requested to exclude the development or persistence of infection such as a collection of  pus. In surgical units in which resistant Pseudomonas or other Gram-negative species (such as Klebsiella ) have become ‘resident opportunists’, it may be necessary to rotate anti pseudomonal and anti-Gram-negative antibiotic therapy ( Summary box 5.15 ). Summary box 5.15 Treatment of commensals that have become opportun ist pathogens /uni25CF /uni25CF 

Antibiotics do not replace surgical drainage of infection
Only spreading infections or signs of systemic infection justify
the use of antibiotics
Whenever possible, the organism and sensitivity should be
determined
They are likely to have multiple antibiotic resistance
It may be necessary to rotate antibiotics

# ANTIMICROBIAL TREATMENT OF SURGICAL INFECTION Principles

ANTIMICROBIAL TREATMENT OF SURGICAL INFECTION Principles

Antimicrobials may be used to prevent or treat established surgical infection. The use of  antibiotics for the treatment of  established surgi - cal infection ideally requires recognition and determination of the sensitivities of  the causative organisms. Antibiotic therapy Figure 5.18 

Infected animal bite/wound of the upper thigh, treated
by open therapy following virulent staphylococcal infection.

empirical and later modified depending on microbiological findings on culture and sensitivity . Once antibiotics have been administered, it may not be possible to grow bacteria from the wound and so the opportunity to ascertain the most appropri ate antibiotic sensitivities is lost if  a patient’s condition does not improve on empirical antibiotic therapy . Antibiotics alone are rarely su ffi cient to treat SSIs, which may also need open drainage and debridement ( Summary box 5.14 ). Summary box 5.14 Principles for the use of antibiotic therapy /uni25CF /uni25CF /uni25CF There are two approaches to antibiotic treatment: A narrow-spectrum antibiotic may be used to treat a known sensitive infection; for example, MRSA (which may be isolated from pus) is usually sensitive to vancomycin or teico planin, but not flucloxacillin. Combinations of broad-spectrum antibiotics can be used when the organism is not known or when it is suspected that several bacteria, acting in synergy , may be responsible for the infection. For example, during and follow ing emergency surgery requiring the opening of  perforated or ischaemic bowel, any of the gut organisms may be responsi b le for subsequent peritoneal or bacteraemic infection. In this case, a broad-spectrum antibiotic such as teicoplanin or mero penem, which are e ff ective against a wide range of  aerobic bacteria, is combined with metronidazole, which is e ff ectiv against anaerobic bacteria. Alternatively , triple therap y is used with amoxicillin, gentamicin and metronidazole. The use of such broad-spectrum antibiotic strategies should be guided by specialist microbiological advice. If  clinical response is poor after 3–4 days, there should be a re-evaluation with a review of  available culture and sensitivity results and further investi gations requested to exclude the development or persistence of infection such as a collection of  pus. In surgical units in which resistant Pseudomonas or other Gram-negative species (such as Klebsiella ) have become ‘resident opportunists’, it may be necessary to rotate anti pseudomonal and anti-Gram-negative antibiotic therapy ( Summary box 5.15 ). Summary box 5.15 Treatment of commensals that have become opportun ist pathogens /uni25CF /uni25CF 

Antibiotics do not replace surgical drainage of infection
Only spreading infections or signs of systemic infection justify
the use of antibiotics
Whenever possible, the organism and sensitivity should be
determined
They are likely to have multiple antibiotic resistance
It may be necessary to rotate antibiotics

# Discovery of antibiotics

Discovery of antibiotics

The concept of  a ‘magic bullet’ ( Zauberkugel ) that could kill microbes but not their host became a reality with the discovery Figure 5.1 Louis Pasteur , 1822–1895, French chemist, bacteriologist and immunologist, Professor of  Chemistry at the Sorbonne, Paris, France. Lord Joseph Lister , 1827–1912, Professor of  Surgery , Glasgow , Scotland (1860–1869), Edinburgh, Scotland (1869–1877) and King’s College Hospital, London, England (1877–1892). Sir Alexander Fleming , 1881–1955, Professor of  Bacteriology , St Mary’s Hospital, London, England, discovered Howard Walter Florey (Lord Florey of  Adelaide) , 1898–1968, Professor of  Pathology , the University of  Oxford, Oxford, England. Sir Ernst Boris Chain , Professor of  Biochemistry , Imperial College, London, England. Fleming, Florey and Chain shared the 1945 Nobel Prize in Physiology or Medicine for their work on penicillin. Hans Christian Joachim Gram , 1853–1938, Professor of  Pharmacology (1891–1900) and of  Medicine (1900–1923), Copenhagen, Denmark, described this method of  staining bacteria in 1884. The discovery of  the antibiotic penicillin is attributed to Alexander Fleming in 1928, but it was not isolated for clinical use until 1941, by Florey and Chain. The first patient to receive penicillin was Police Constable Alexander in Oxford. Since then there has been a proliferation of antibiotics with broad-spectrum activity and antibiotics today remain the mainstay of  antimicrobial therapy . 

(a)
Aseptic techniques of scrubbing and draping in a modern operating theatre.

Discovery of antibiotics

The concept of  a ‘magic bullet’ ( Zauberkugel ) that could kill microbes but not their host became a reality with the discovery Figure 5.1 Louis Pasteur , 1822–1895, French chemist, bacteriologist and immunologist, Professor of  Chemistry at the Sorbonne, Paris, France. Lord Joseph Lister , 1827–1912, Professor of  Surgery , Glasgow , Scotland (1860–1869), Edinburgh, Scotland (1869–1877) and King’s College Hospital, London, England (1877–1892). Sir Alexander Fleming , 1881–1955, Professor of  Bacteriology , St Mary’s Hospital, London, England, discovered Howard Walter Florey (Lord Florey of  Adelaide) , 1898–1968, Professor of  Pathology , the University of  Oxford, Oxford, England. Sir Ernst Boris Chain , Professor of  Biochemistry , Imperial College, London, England. Fleming, Florey and Chain shared the 1945 Nobel Prize in Physiology or Medicine for their work on penicillin. Hans Christian Joachim Gram , 1853–1938, Professor of  Pharmacology (1891–1900) and of  Medicine (1900–1923), Copenhagen, Denmark, described this method of  staining bacteria in 1884. The discovery of  the antibiotic penicillin is attributed to Alexander Fleming in 1928, but it was not isolated for clinical use until 1941, by Florey and Chain. The first patient to receive penicillin was Police Constable Alexander in Oxford. Since then there has been a proliferation of antibiotics with broad-spectrum activity and antibiotics today remain the mainstay of  antimicrobial therapy . 

(a)
Aseptic techniques of scrubbing and draping in a modern operating theatre.

Discovery of antibiotics

The concept of  a ‘magic bullet’ ( Zauberkugel ) that could kill microbes but not their host became a reality with the discovery Figure 5.1 Louis Pasteur , 1822–1895, French chemist, bacteriologist and immunologist, Professor of  Chemistry at the Sorbonne, Paris, France. Lord Joseph Lister , 1827–1912, Professor of  Surgery , Glasgow , Scotland (1860–1869), Edinburgh, Scotland (1869–1877) and King’s College Hospital, London, England (1877–1892). Sir Alexander Fleming , 1881–1955, Professor of  Bacteriology , St Mary’s Hospital, London, England, discovered Howard Walter Florey (Lord Florey of  Adelaide) , 1898–1968, Professor of  Pathology , the University of  Oxford, Oxford, England. Sir Ernst Boris Chain , Professor of  Biochemistry , Imperial College, London, England. Fleming, Florey and Chain shared the 1945 Nobel Prize in Physiology or Medicine for their work on penicillin. Hans Christian Joachim Gram , 1853–1938, Professor of  Pharmacology (1891–1900) and of  Medicine (1900–1923), Copenhagen, Denmark, described this method of  staining bacteria in 1884. The discovery of  the antibiotic penicillin is attributed to Alexander Fleming in 1928, but it was not isolated for clinical use until 1941, by Florey and Chain. The first patient to receive penicillin was Police Constable Alexander in Oxford. Since then there has been a proliferation of antibiotics with broad-spectrum activity and antibiotics today remain the mainstay of  antimicrobial therapy . 

(a)
Aseptic techniques of scrubbing and draping in a modern operating theatre.

# FURTHER READING

FURTHER READING

Fraise AP , Bradley C. Ayli ff e’s control of  healthcare associated infection: a practical handbook. London: Hodder Arnold, 2009. Fry DE. Surgical infections. London: JP Medical Ltd, 2013. Sawyer RG, Hedrick TL. Surgical infections, an issue of  surgical clinics. New Y ork: Elsevier –Health Sciences Division, 2014. Thomas WEG, Reed MWR, Wyatt MG. Oxford textbook of  fundamentals of  surgery. Oxford: Oxford University Press, 2016. Torok E, Moran E, Cooke F . Oxford handbook of  infectious diseases and microbiology , 2nd edn. Oxford: Oxford University Press, 2016. FURTHER READING

Fraise AP , Bradley C. Ayli ff e’s control of  healthcare associated infection: a practical handbook. London: Hodder Arnold, 2009. Fry DE. Surgical infections. London: JP Medical Ltd, 2013. Sawyer RG, Hedrick TL. Surgical infections, an issue of  surgical clinics. New Y ork: Elsevier –Health Sciences Division, 2014. Thomas WEG, Reed MWR, Wyatt MG. Oxford textbook of  fundamentals of  surgery. Oxford: Oxford University Press, 2016. Torok E, Moran E, Cooke F . Oxford handbook of  infectious diseases and microbiology , 2nd edn. Oxford: Oxford University Press, 2016. FURTHER READING

Fraise AP , Bradley C. Ayli ff e’s control of  healthcare associated infection: a practical handbook. London: Hodder Arnold, 2009. Fry DE. Surgical infections. London: JP Medical Ltd, 2013. Sawyer RG, Hedrick TL. Surgical infections, an issue of  surgical clinics. New Y ork: Elsevier –Health Sciences Division, 2014. Thomas WEG, Reed MWR, Wyatt MG. Oxford textbook of  fundamentals of  surgery. Oxford: Oxford University Press, 2016. Torok E, Moran E, Cooke F . Oxford handbook of  infectious diseases and microbiology , 2nd edn. Oxford: Oxford University Press, 2016.

# HISTORY OF SURGICAL INFECTION Background

HISTORY OF SURGICAL INFECTION Background

Surgical infections have always been a major complication related to surgery and trauma and have been documented for 4000–5000 years. Egyptians popularised some concepts about infection, as they were able to prevent putrefaction using their skills in mummification. Their medical papyruses also describe the use of  salves and antiseptics to prevent surgical site infec tions (SSIs). This ‘prophylaxis’ had also been known earlier by the Assyrians, although it is less well documented. It was described again independently by the Greeks. The Hippocratic teachings described the use of antimicrobials, such as wine and vinegar, w hich were widely used to irrigate open, infected wounds before delayed primary or secondary wound closure. A belief  common to all these civilisations, and indeed even later to the Romans, was that Hippocrates of  Kos , Greek physician and surgeon, and by common consent ‘the father of medicine’, was born on the island of  Kos, o ff Turkey , about 460 /uni00A0/b.sc/c.sc/e.sc and probably died in 375 /uni00A0 /b.sc/c.sc/e.sc . Galen , 130–200, Roman physician, commenced practice as Surgeon to the Gladiators at Pergamum (now Bergama in Turkey) and later became personal physician to the Emperor Marcus Aurelius. As a prolific writer in anatomy , medicine, pathology and philosophy , his work a ff ected medical thinking for 15 centuries after his death. (Gladiator is Latin for ‘swordsman’.) Theodoric of  Cervia , 1210–1298, Bishop of  Cervia, published a book on surgery ca. 1267. Ambroise Paré , 1510–1590, French military surgeon, also worked at the Hotel Dieu, Paris, France. Guy de Chauliac , 1298–1368, physician and chaplain to Pope Clement VI at Avignon, France, and the author of Robert Koch , 1843–1910, Professor of  Hygiene and Bacteriology , Berlin, Germany , stated his ‘Postulates’ in 1882. Ignaz Semmelweis , 1818–1865, Professor of  Obstetrics, Budapest, Hungary . whenever pus was localised in an infected wound it needed to be drained. Galen recognised that this localisation of  infection (sup - puration) in wounds inflicted in the gladiatorial arena often heralded recovery , particularly after drainage ( pus bonum et laudabile ) . Theodoric of  Cervia, Ambroise Paré and Guy de Chauliac observed that clean wounds, closed primarily , could heal without infection or suppuration. - 

To learn:
Koch’s postulates
•
The management of abscesses
•
The Surviving Sepsis Campaign, sepsis bundle and
•
Sepsis Six
Surgical implications of the COVID-19 pandemic
•
To appreciate:
The importance of aseptic and antiseptic techniques and
•
delayed primary or secondary closure in contaminated
wounds
To be aware of:
The causes of reduced resistance to infection (host
•
response)
To know:
The de
/f_i
nitions of infection, particularly at surgical sites
•
What basic precautions to take to avoid surgically relevant
•
hospital-acquired infections

HISTORY OF SURGICAL INFECTION Background

Surgical infections have always been a major complication related to surgery and trauma and have been documented for 4000–5000 years. Egyptians popularised some concepts about infection, as they were able to prevent putrefaction using their skills in mummification. Their medical papyruses also describe the use of  salves and antiseptics to prevent surgical site infec tions (SSIs). This ‘prophylaxis’ had also been known earlier by the Assyrians, although it is less well documented. It was described again independently by the Greeks. The Hippocratic teachings described the use of antimicrobials, such as wine and vinegar, w hich were widely used to irrigate open, infected wounds before delayed primary or secondary wound closure. A belief  common to all these civilisations, and indeed even later to the Romans, was that Hippocrates of  Kos , Greek physician and surgeon, and by common consent ‘the father of medicine’, was born on the island of  Kos, o ff Turkey , about 460 /uni00A0/b.sc/c.sc/e.sc and probably died in 375 /uni00A0 /b.sc/c.sc/e.sc . Galen , 130–200, Roman physician, commenced practice as Surgeon to the Gladiators at Pergamum (now Bergama in Turkey) and later became personal physician to the Emperor Marcus Aurelius. As a prolific writer in anatomy , medicine, pathology and philosophy , his work a ff ected medical thinking for 15 centuries after his death. (Gladiator is Latin for ‘swordsman’.) Theodoric of  Cervia , 1210–1298, Bishop of  Cervia, published a book on surgery ca. 1267. Ambroise Paré , 1510–1590, French military surgeon, also worked at the Hotel Dieu, Paris, France. Guy de Chauliac , 1298–1368, physician and chaplain to Pope Clement VI at Avignon, France, and the author of Robert Koch , 1843–1910, Professor of  Hygiene and Bacteriology , Berlin, Germany , stated his ‘Postulates’ in 1882. Ignaz Semmelweis , 1818–1865, Professor of  Obstetrics, Budapest, Hungary . whenever pus was localised in an infected wound it needed to be drained. Galen recognised that this localisation of  infection (sup - puration) in wounds inflicted in the gladiatorial arena often heralded recovery , particularly after drainage ( pus bonum et laudabile ) . Theodoric of  Cervia, Ambroise Paré and Guy de Chauliac observed that clean wounds, closed primarily , could heal without infection or suppuration. - 

To learn:
Koch’s postulates
•
The management of abscesses
•
The Surviving Sepsis Campaign, sepsis bundle and
•
Sepsis Six
Surgical implications of the COVID-19 pandemic
•
To appreciate:
The importance of aseptic and antiseptic techniques and
•
delayed primary or secondary closure in contaminated
wounds
To be aware of:
The causes of reduced resistance to infection (host
•
response)
To know:
The de
/f_i
nitions of infection, particularly at surgical sites
•
What basic precautions to take to avoid surgically relevant
•
hospital-acquired infections

HISTORY OF SURGICAL INFECTION Background

Surgical infections have always been a major complication related to surgery and trauma and have been documented for 4000–5000 years. Egyptians popularised some concepts about infection, as they were able to prevent putrefaction using their skills in mummification. Their medical papyruses also describe the use of  salves and antiseptics to prevent surgical site infec tions (SSIs). This ‘prophylaxis’ had also been known earlier by the Assyrians, although it is less well documented. It was described again independently by the Greeks. The Hippocratic teachings described the use of antimicrobials, such as wine and vinegar, w hich were widely used to irrigate open, infected wounds before delayed primary or secondary wound closure. A belief  common to all these civilisations, and indeed even later to the Romans, was that Hippocrates of  Kos , Greek physician and surgeon, and by common consent ‘the father of medicine’, was born on the island of  Kos, o ff Turkey , about 460 /uni00A0/b.sc/c.sc/e.sc and probably died in 375 /uni00A0 /b.sc/c.sc/e.sc . Galen , 130–200, Roman physician, commenced practice as Surgeon to the Gladiators at Pergamum (now Bergama in Turkey) and later became personal physician to the Emperor Marcus Aurelius. As a prolific writer in anatomy , medicine, pathology and philosophy , his work a ff ected medical thinking for 15 centuries after his death. (Gladiator is Latin for ‘swordsman’.) Theodoric of  Cervia , 1210–1298, Bishop of  Cervia, published a book on surgery ca. 1267. Ambroise Paré , 1510–1590, French military surgeon, also worked at the Hotel Dieu, Paris, France. Guy de Chauliac , 1298–1368, physician and chaplain to Pope Clement VI at Avignon, France, and the author of Robert Koch , 1843–1910, Professor of  Hygiene and Bacteriology , Berlin, Germany , stated his ‘Postulates’ in 1882. Ignaz Semmelweis , 1818–1865, Professor of  Obstetrics, Budapest, Hungary . whenever pus was localised in an infected wound it needed to be drained. Galen recognised that this localisation of  infection (sup - puration) in wounds inflicted in the gladiatorial arena often heralded recovery , particularly after drainage ( pus bonum et laudabile ) . Theodoric of  Cervia, Ambroise Paré and Guy de Chauliac observed that clean wounds, closed primarily , could heal without infection or suppuration. - 

To learn:
Koch’s postulates
•
The management of abscesses
•
The Surviving Sepsis Campaign, sepsis bundle and
•
Sepsis Six
Surgical implications of the COVID-19 pandemic
•
To appreciate:
The importance of aseptic and antiseptic techniques and
•
delayed primary or secondary closure in contaminated
wounds
To be aware of:
The causes of reduced resistance to infection (host
•
response)
To know:
The de
/f_i
nitions of infection, particularly at surgical sites
•
What basic precautions to take to avoid surgically relevant
•
hospital-acquired infections

# INFECTION Preoperative preparation

INFECTION Preoperative preparation

A short preoperative hospital stay lowers the risk of  acquiring MRSA, multidrug-resistant coagulase-negative staphylococci and other antibiotic-resistant organisms from the hospital environment. Medical and nursing sta ff should always wash their hands after any patient contact. Hand gels containing at least 70% alcohol can act as a substitute for handwashing, but do not destroy the spores of C. di ff ., which may cause pseudo- membranous colitis, especially in immunocompromised patients or those whose gut flora is suppressed by antibiotic therapy . Although the need for clean hospitals, emphasised by the media, is logical, the ‘clean your hands campaign’, particu larly in the COVID-19 era, is beginning to result in falls in the incidence of  HAIs. Sta ff with open, infected skin lesions should not enter the operating theatres. Ideally , neither should a ff ected patients, especially if  they are having a prosthesis implanted. Antiseptic baths (usually c hlorhexidine) are popular in Europe, but there is no hard evidence for their value in reducing wound infections. Preoperative skin shaving should be undertaken in the operating theatre immediately before surgery as the SSI rate after clean wound surgery may be doubled if  shaving is performed the night before because minor skin injury enhances superficial bacterial colonisation. Scrubbing and skin preparation When washing the hands prior to surgery , dilute alcohol-based antiseptic hand soaps such as chlorhexidine or povidone– iodine should be used, and the scrub should include the nails ( Figure 5.1 ) . One application of  a more concentrated alcohol-based antiseptic is adequate for skin preparation of  the operative site. This leads to a >95% reduction in bacterial count but caution should be taken not to leave a pool of  alcohol-based fluid on the skin as it could ignite with diather my and burn the patient ( Figure 5.1 ) . Theatre technique and discipline also contribute to low infection rates. Numbers of  sta ff in the theatre and movement in and out of  theatre should be kept to a minimum. Careful and regular surveillance is needed to ensure the quality of ment sterilisation, aseptic technique and theatre ventilation. Laminar flow systems direct clean, filtered air over the operat ing field, with any air potentially contaminated as it passes over the incision then directed away from the patient. Operator skill in gentle manipula tion and dissection of  tissues is much more di ffi cult to audit, but dead spaces and haematomas should be avoided. T here is no evidence that drains, incision drapes or wound guards help to reduce wound infection. There is a high level of  evidence that both the perioperative avoidance of  hypothermia and the use of  supplemental oxygen during recovery significantly reduce the rate of  SSIs. INFECTION Preoperative preparation

A short preoperative hospital stay lowers the risk of  acquiring MRSA, multidrug-resistant coagulase-negative staphylococci and other antibiotic-resistant organisms from the hospital environment. Medical and nursing sta ff should always wash their hands after any patient contact. Hand gels containing at least 70% alcohol can act as a substitute for handwashing, but do not destroy the spores of C. di ff ., which may cause pseudo- membranous colitis, especially in immunocompromised patients or those whose gut flora is suppressed by antibiotic therapy . Although the need for clean hospitals, emphasised by the media, is logical, the ‘clean your hands campaign’, particu larly in the COVID-19 era, is beginning to result in falls in the incidence of  HAIs. Sta ff with open, infected skin lesions should not enter the operating theatres. Ideally , neither should a ff ected patients, especially if  they are having a prosthesis implanted. Antiseptic baths (usually c hlorhexidine) are popular in Europe, but there is no hard evidence for their value in reducing wound infections. Preoperative skin shaving should be undertaken in the operating theatre immediately before surgery as the SSI rate after clean wound surgery may be doubled if  shaving is performed the night before because minor skin injury enhances superficial bacterial colonisation. Scrubbing and skin preparation When washing the hands prior to surgery , dilute alcohol-based antiseptic hand soaps such as chlorhexidine or povidone– iodine should be used, and the scrub should include the nails ( Figure 5.1 ) . One application of  a more concentrated alcohol-based antiseptic is adequate for skin preparation of  the operative site. This leads to a >95% reduction in bacterial count but caution should be taken not to leave a pool of  alcohol-based fluid on the skin as it could ignite with diather my and burn the patient ( Figure 5.1 ) . Theatre technique and discipline also contribute to low infection rates. Numbers of  sta ff in the theatre and movement in and out of  theatre should be kept to a minimum. Careful and regular surveillance is needed to ensure the quality of ment sterilisation, aseptic technique and theatre ventilation. Laminar flow systems direct clean, filtered air over the operat ing field, with any air potentially contaminated as it passes over the incision then directed away from the patient. Operator skill in gentle manipula tion and dissection of  tissues is much more di ffi cult to audit, but dead spaces and haematomas should be avoided. T here is no evidence that drains, incision drapes or wound guards help to reduce wound infection. There is a high level of  evidence that both the perioperative avoidance of  hypothermia and the use of  supplemental oxygen during recovery significantly reduce the rate of  SSIs. INFECTION Preoperative preparation

A short preoperative hospital stay lowers the risk of  acquiring MRSA, multidrug-resistant coagulase-negative staphylococci and other antibiotic-resistant organisms from the hospital environment. Medical and nursing sta ff should always wash their hands after any patient contact. Hand gels containing at least 70% alcohol can act as a substitute for handwashing, but do not destroy the spores of C. di ff ., which may cause pseudo- membranous colitis, especially in immunocompromised patients or those whose gut flora is suppressed by antibiotic therapy . Although the need for clean hospitals, emphasised by the media, is logical, the ‘clean your hands campaign’, particu larly in the COVID-19 era, is beginning to result in falls in the incidence of  HAIs. Sta ff with open, infected skin lesions should not enter the operating theatres. Ideally , neither should a ff ected patients, especially if  they are having a prosthesis implanted. Antiseptic baths (usually c hlorhexidine) are popular in Europe, but there is no hard evidence for their value in reducing wound infections. Preoperative skin shaving should be undertaken in the operating theatre immediately before surgery as the SSI rate after clean wound surgery may be doubled if  shaving is performed the night before because minor skin injury enhances superficial bacterial colonisation. Scrubbing and skin preparation When washing the hands prior to surgery , dilute alcohol-based antiseptic hand soaps such as chlorhexidine or povidone– iodine should be used, and the scrub should include the nails ( Figure 5.1 ) . One application of  a more concentrated alcohol-based antiseptic is adequate for skin preparation of  the operative site. This leads to a >95% reduction in bacterial count but caution should be taken not to leave a pool of  alcohol-based fluid on the skin as it could ignite with diather my and burn the patient ( Figure 5.1 ) . Theatre technique and discipline also contribute to low infection rates. Numbers of  sta ff in the theatre and movement in and out of  theatre should be kept to a minimum. Careful and regular surveillance is needed to ensure the quality of ment sterilisation, aseptic technique and theatre ventilation. Laminar flow systems direct clean, filtered air over the operat ing field, with any air potentially contaminated as it passes over the incision then directed away from the patient. Operator skill in gentle manipula tion and dissection of  tissues is much more di ffi cult to audit, but dead spaces and haematomas should be avoided. T here is no evidence that drains, incision drapes or wound guards help to reduce wound infection. There is a high level of  evidence that both the perioperative avoidance of  hypothermia and the use of  supplemental oxygen during recovery significantly reduce the rate of  SSIs.

# Introduction

## Introduction

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# Koch’s postulates

Koch’s postulates

An understanding of  the causes of  infection came in the nine - teenth century . Microbes had been seen under the microscope, but Koch laid down the first definition of  infective disease (Koch’s postula tes; see Summary box 5.1 ). The Austrian obstetrician Ignaz Semmelweis showed that puerperal sepsis could be reduced from an incidence of  over Chirurgia Magna, which was published about 1363. Koch’s postulates proving whether a given organism is the cause of a given disease /uni25CF /uni25CF /uni25CF /uni25CF 10% to under 2% by the simple act of  handwashing between cases, particularly between postmortem examinations and the delivery suite. Louis Pasteur recognised through his germ theory that microorganisms were responsible for infecting humans and causing disease. Joseph Lister applied this knowledge to the reduction of  colonising organisms in compound fractures b using antiseptics. The principles of  antiseptic surgery were soon enhanced with aseptic surgery at the turn of  the twenti eth century . As well as killing the bacteria on the skin before surgical incision (antiseptic technique), the conditions under which the operation was performed were kept free of  bacteria (aseptic technique). This technique is still emplo yed in modern operating theatres ( Figure 5.1 ). 

It must be found in every case
It should be possible to isolate it from the host and grow it in
culture
It should reproduce the disease when injected into another
healthy host
It should be recovered from an experimentally infected host

Koch’s postulates

An understanding of  the causes of  infection came in the nine - teenth century . Microbes had been seen under the microscope, but Koch laid down the first definition of  infective disease (Koch’s postula tes; see Summary box 5.1 ). The Austrian obstetrician Ignaz Semmelweis showed that puerperal sepsis could be reduced from an incidence of  over Chirurgia Magna, which was published about 1363. Koch’s postulates proving whether a given organism is the cause of a given disease /uni25CF /uni25CF /uni25CF /uni25CF 10% to under 2% by the simple act of  handwashing between cases, particularly between postmortem examinations and the delivery suite. Louis Pasteur recognised through his germ theory that microorganisms were responsible for infecting humans and causing disease. Joseph Lister applied this knowledge to the reduction of  colonising organisms in compound fractures b using antiseptics. The principles of  antiseptic surgery were soon enhanced with aseptic surgery at the turn of  the twenti eth century . As well as killing the bacteria on the skin before surgical incision (antiseptic technique), the conditions under which the operation was performed were kept free of  bacteria (aseptic technique). This technique is still emplo yed in modern operating theatres ( Figure 5.1 ). 

It must be found in every case
It should be possible to isolate it from the host and grow it in
culture
It should reproduce the disease when injected into another
healthy host
It should be recovered from an experimentally infected host

Koch’s postulates

An understanding of  the causes of  infection came in the nine - teenth century . Microbes had been seen under the microscope, but Koch laid down the first definition of  infective disease (Koch’s postula tes; see Summary box 5.1 ). The Austrian obstetrician Ignaz Semmelweis showed that puerperal sepsis could be reduced from an incidence of  over Chirurgia Magna, which was published about 1363. Koch’s postulates proving whether a given organism is the cause of a given disease /uni25CF /uni25CF /uni25CF /uni25CF 10% to under 2% by the simple act of  handwashing between cases, particularly between postmortem examinations and the delivery suite. Louis Pasteur recognised through his germ theory that microorganisms were responsible for infecting humans and causing disease. Joseph Lister applied this knowledge to the reduction of  colonising organisms in compound fractures b using antiseptics. The principles of  antiseptic surgery were soon enhanced with aseptic surgery at the turn of  the twenti eth century . As well as killing the bacteria on the skin before surgical incision (antiseptic technique), the conditions under which the operation was performed were kept free of  bacteria (aseptic technique). This technique is still emplo yed in modern operating theatres ( Figure 5.1 ). 

It must be found in every case
It should be possible to isolate it from the host and grow it in
culture
It should reproduce the disease when injected into another
healthy host
It should be recovered from an experimentally infected host

# Learning objectives

Learning objectives

To understand: The characteristics of the common surgical pathogens • and their sensitivities The factors that determine whether a wound will become • infected The classi /f_i cation of sources of infection and their severity • The clinical presentation of surgical infections • The indications for and choice of prophylactic antibiotics • The spectrum of commonly used antibiotics in surgery • and principles of therapy The misuse of antibiotic therapy with the risk of resistance • to antibiotics (such as methicillin-resistant Staphylococcus aureus [MRSA]) and emergence of resistant strains (such as Clostridium dif /f_i cile enteritis) Learning objectives

To understand: The characteristics of the common surgical pathogens • and their sensitivities The factors that determine whether a wound will become • infected The classi /f_i cation of sources of infection and their severity • The clinical presentation of surgical infections • The indications for and choice of prophylactic antibiotics • The spectrum of commonly used antibiotics in surgery • and principles of therapy The misuse of antibiotic therapy with the risk of resistance • to antibiotics (such as methicillin-resistant Staphylococcus aureus [MRSA]) and emergence of resistant strains (such as Clostridium dif /f_i cile enteritis) Learning objectives

To understand: The characteristics of the common surgical pathogens • and their sensitivities The factors that determine whether a wound will become • infected The classi /f_i cation of sources of infection and their severity • The clinical presentation of surgical infections • The indications for and choice of prophylactic antibiotics • The spectrum of commonly used antibiotics in surgery • and principles of therapy The misuse of antibiotic therapy with the risk of resistance • to antibiotics (such as methicillin-resistant Staphylococcus aureus [MRSA]) and emergence of resistant strains (such as Clostridium dif /f_i cile enteritis)

# MICROBIOLOGY OF SURGICAL INFECTION Common bacteria involved in surgical infections

MICROBIOLOGY OF SURGICAL INFECTION Common bacteria involved in surgical infections

Streptococci Streptococci form chains and are Gram positive on staining ( Figure 5.2a ). The most important is the β -haemolytic Streptococcus , which resides in the pharynx of  5–10% of  the Figure 5.2 (a) (b) Rebecca Graighill Lancefield , 1895–1981, American bacteriologist, classified streptococci in 1933. - sification, it is the group A Streptococcus, also called Streptococcus pyogenes, that is the most pathogenic. It has the ability to spread, causing cellulitis, and to cause tissue destruction through the ). release of enzymes such as streptolysin, streptokinase and streptodornase. Streptococcus faecalis is an enterococcus in Lancefield group D. It is often found in synergy with other organisms, as are the γ -haemolytic Streptococcus and Peptostreptococcus , which is an anaerobe. Both Streptococcus pyogenes and Streptococcus faecalis may be involved in wound infection after bowel surgery , but the α -haemolytic Streptococcus viridans is not associated with wound infections. All the streptococci remain sensitive to penicillin and erythromycin. The cephalosporins are a suitable alternative in patients who are allergic to penicillin. Staphylococci Staphylococci form clumps and are Gram positive ( Figure 5.2b ). Staphylococcus aureus is the most important pathogen in - this group and is found in the nasopharynx of  up to 15% of  the population. It can cause suppuration in wounds and around implanted prostheses. Some strains are resistant to many common antibiotics (especially MRSA) and so are di ffi cult to treat. MRSA can be found in the nose of asymptomatic carriers among both patients and hospital workers, a potential source of infection after surgery . In parts of northern Europe, the prevalence of MRSA infections has been kept at very low levels using ‘search and destroy’ methods, which use screening techniques to look for MRSA in patients before they come in to hospital for elective surgery so that any carriers can be treated before their admission for surgery . Local policies on the management of  MRSA depend on the prevalence of  MRSA, the type of hospital, the clinical specialty and the availability of  facilities. Widespread swabbing, ward closures, isolation of patients and disinfection of  wards by deep cleaning must all be carefully considered. 

(a)
Streptococci.
Staphylococcal pus.
(b)

Figure 5.3 Staphylococcal infections are usually suppurative and localised. Most hospital Staphylococcus aureus strains are now β -lactamase producers and so are resistant to penicillin, but many strains remain sensitive to flucloxacillin, vancomycin, aminoglycosides and some cephalosporins. Nowadays, sev eral novel and innovative antibiotics have become available that have high activity against resistant strains. Some have the advantage of  good oral activity (linezolid), some have a wide spectrum (teicoplanin), some have good activity in bacteraemia (daptomy cin) but all are relatively expensive, and some have side e ff ects involving marrow , hepatic and renal toxicity . Their use is justified but needs to be controlled by tight local policies and guidelines that involve clinical microbiologists. Staphylococcus epidermidis (previously Staphylococcus albus also known as coagulase-negative Staphylococcus , was regarded as a non-pathogenic commensal organism commonly found on the skin, but is now recognised as a major threat in vascular and orthopaedic prosthetic surgery and in indwelling vascular cannulae/catheters. The bacteria form biofilms that adhere to prosthetic surfaces and limit the e ff ectiveness of  antibiotics. Clostridia Clostridial organisms are Gram-positive, obligate anaerobes that produce resistant spores ( Figure 5.3 ). Clostridium perfrin gens is the cause of  gas gangrene, and Clostridium tetani tetanus. Clostridium di ffi cile ( C. di ff . ) is the cause of  pseudomem branous colitis, in which destruction of  the normal colonic bacterial flora by antibiotic therapy allows an overgrowth of the normal gut commensal C. di ff . to pathological levels. Any antibiotic may cause this phenomenon, although the quino lones such as ciprofloxacin seem to be the highest risk, espe cially in elderly or immunocompromised patients. In its most severe form, the colitis may lead to perforation and the need for emergency colectomy with an associated high mortality . Treatment in volves resuscitation and antibiotic therapy . The fibrinous exudate is typical and di ff erentiates the colitis from other inflammatory diseases. Theodor Escherich, 1857–1911 , Professor of  Paediatrics, Vienna, Austria, discovered the Bacterium coli commune in 1886. Theodor Albrecht Edwin Klebs , 1834–1913, Professor of  Bacteriology successively at Prague, Czechoslovakia, Zurich, Switzerland and The Rush Medical College, Chicago, IL, USA. ing either C. di ff . glutamate dehydrogenase (GDH) antigen or C. di ff . toxin A/B. The Clostridium di ffi cile GDH Ag Rapid test qualitatively detects for the presence of C. di ff . GDH antigen in faeces. On the other hand, the Clostridium di ffi cile Toxin A/B rapid test qualitatively detects for the presence of C. di ff . toxins A and B in faeces. These rapid tests apply lateral flow immuno - chromatography and are for professional in vitro diagnostic use. Results are usually returned from this rapid testing in less than 30 minutes. Empirical treatment with metronidazole or vancomycin is recommended while awaiting results. Aerobic Gram-negative bacilli These bacilli are normal inhabitants of  the large bowel. Esch - erichia coli and Klebsiella spp. are lactose fermenting; Proteus is non-lactose fermenting. Most organisms in this group act in synergy with Bacteroides to cause SSIs after bowel operations (in particular, appendicitis, diverticulitis and peritonitis). Esch - erichia coli is a major cause of  urinary tract infection, although most aerobic Gram-negative bacilli can be involved, particu - larly in relation to urinary catheterisation. There is increasing concern about the development of  ESBLs in many of  this - group of  bacteria, which confer resistance to many antibiotics, particularly cephalosporins . Pseudomonas spp. tend to colonise burns and tracheostomy wounds, as well as the urinary tract. Once Pseudomonas has colonised wards and intensive care units (ICUs), it may be dif - ficult to eradicate. Surveillance of cross-infection is important in outbreaks. Hospital strains become resistant to β -lactamase as resistance can be transferred by plasmids. Wound infec - tions need antibiotic therapy only when there is prog ressive or ), spreading infection with systemic signs. The aminoglycosides and the quinolones are e ff ective, but some cephalosporins and penicillin ma y not be. Many of  the carbapenems (e.g. mero - penem) are useful in severe infections. Bacteroides Bacteroides are non-spore-bearing, strict anaerobes that colonise the large bowel, vagina and oropharynx. Bacteroides fragilis is the principal organism that acts in synergy with aerobic Gram- - negative bacilli to cause SSIs, including intra-abdominal causes abscesses after colorectal or gynaecological surgery . They are sensitive to the imidazoles (e.g. metronidazole) and some - cephalosporins (e.g. cefotaxime). 

Clostridium tetani
(drumstick spores).

# MICROBIOLOGY OF SURGICAL INFECTION Common bacteria

MICROBIOLOGY OF SURGICAL INFECTION Common bacteria involved in surgical infections

Streptococci Streptococci form chains and are Gram positive on staining ( Figure 5.2a ). The most important is the β -haemolytic Streptococcus , which resides in the pharynx of  5–10% of  the Figure 5.2 (a) (b) Rebecca Graighill Lancefield , 1895–1981, American bacteriologist, classified streptococci in 1933. - sification, it is the group A Streptococcus, also called Streptococcus pyogenes, that is the most pathogenic. It has the ability to spread, causing cellulitis, and to cause tissue destruction through the ). release of enzymes such as streptolysin, streptokinase and streptodornase. Streptococcus faecalis is an enterococcus in Lancefield group D. It is often found in synergy with other organisms, as are the γ -haemolytic Streptococcus and Peptostreptococcus , which is an anaerobe. Both Streptococcus pyogenes and Streptococcus faecalis may be involved in wound infection after bowel surgery , but the α -haemolytic Streptococcus viridans is not associated with wound infections. All the streptococci remain sensitive to penicillin and erythromycin. The cephalosporins are a suitable alternative in patients who are allergic to penicillin. Staphylococci Staphylococci form clumps and are Gram positive ( Figure 5.2b ). Staphylococcus aureus is the most important pathogen in - this group and is found in the nasopharynx of  up to 15% of  the population. It can cause suppuration in wounds and around implanted prostheses. Some strains are resistant to many common antibiotics (especially MRSA) and so are di ffi cult to treat. MRSA can be found in the nose of asymptomatic carriers among both patients and hospital workers, a potential source of infection after surgery . In parts of northern Europe, the prevalence of MRSA infections has been kept at very low levels using ‘search and destroy’ methods, which use screening techniques to look for MRSA in patients before they come in to hospital for elective surgery so that any carriers can be treated before their admission for surgery . Local policies on the management of  MRSA depend on the prevalence of  MRSA, the type of hospital, the clinical specialty and the availability of  facilities. Widespread swabbing, ward closures, isolation of patients and disinfection of  wards by deep cleaning must all be carefully considered. 

(a)
Streptococci.
Staphylococcal pus.
(b)

Figure 5.3 Staphylococcal infections are usually suppurative and localised. Most hospital Staphylococcus aureus strains are now β -lactamase producers and so are resistant to penicillin, but many strains remain sensitive to flucloxacillin, vancomycin, aminoglycosides and some cephalosporins. Nowadays, sev eral novel and innovative antibiotics have become available that have high activity against resistant strains. Some have the advantage of  good oral activity (linezolid), some have a wide spectrum (teicoplanin), some have good activity in bacteraemia (daptomy cin) but all are relatively expensive, and some have side e ff ects involving marrow , hepatic and renal toxicity . Their use is justified but needs to be controlled by tight local policies and guidelines that involve clinical microbiologists. Staphylococcus epidermidis (previously Staphylococcus albus also known as coagulase-negative Staphylococcus , was regarded as a non-pathogenic commensal organism commonly found on the skin, but is now recognised as a major threat in vascular and orthopaedic prosthetic surgery and in indwelling vascular cannulae/catheters. The bacteria form biofilms that adhere to prosthetic surfaces and limit the e ff ectiveness of  antibiotics. Clostridia Clostridial organisms are Gram-positive, obligate anaerobes that produce resistant spores ( Figure 5.3 ). Clostridium perfrin gens is the cause of  gas gangrene, and Clostridium tetani tetanus. Clostridium di ffi cile ( C. di ff . ) is the cause of  pseudomem branous colitis, in which destruction of  the normal colonic bacterial flora by antibiotic therapy allows an overgrowth of the normal gut commensal C. di ff . to pathological levels. Any antibiotic may cause this phenomenon, although the quino lones such as ciprofloxacin seem to be the highest risk, espe cially in elderly or immunocompromised patients. In its most severe form, the colitis may lead to perforation and the need for emergency colectomy with an associated high mortality . Treatment in volves resuscitation and antibiotic therapy . The fibrinous exudate is typical and di ff erentiates the colitis from other inflammatory diseases. Theodor Escherich, 1857–1911 , Professor of  Paediatrics, Vienna, Austria, discovered the Bacterium coli commune in 1886. Theodor Albrecht Edwin Klebs , 1834–1913, Professor of  Bacteriology successively at Prague, Czechoslovakia, Zurich, Switzerland and The Rush Medical College, Chicago, IL, USA. ing either C. di ff . glutamate dehydrogenase (GDH) antigen or C. di ff . toxin A/B. The Clostridium di ffi cile GDH Ag Rapid test qualitatively detects for the presence of C. di ff . GDH antigen in faeces. On the other hand, the Clostridium di ffi cile Toxin A/B rapid test qualitatively detects for the presence of C. di ff . toxins A and B in faeces. These rapid tests apply lateral flow immuno - chromatography and are for professional in vitro diagnostic use. Results are usually returned from this rapid testing in less than 30 minutes. Empirical treatment with metronidazole or vancomycin is recommended while awaiting results. Aerobic Gram-negative bacilli These bacilli are normal inhabitants of  the large bowel. Esch - erichia coli and Klebsiella spp. are lactose fermenting; Proteus is non-lactose fermenting. Most organisms in this group act in synergy with Bacteroides to cause SSIs after bowel operations (in particular, appendicitis, diverticulitis and peritonitis). Esch - erichia coli is a major cause of  urinary tract infection, although most aerobic Gram-negative bacilli can be involved, particu - larly in relation to urinary catheterisation. There is increasing concern about the development of  ESBLs in many of  this - group of  bacteria, which confer resistance to many antibiotics, particularly cephalosporins . Pseudomonas spp. tend to colonise burns and tracheostomy wounds, as well as the urinary tract. Once Pseudomonas has colonised wards and intensive care units (ICUs), it may be dif - ficult to eradicate. Surveillance of cross-infection is important in outbreaks. Hospital strains become resistant to β -lactamase as resistance can be transferred by plasmids. Wound infec - tions need antibiotic therapy only when there is prog ressive or ), spreading infection with systemic signs. The aminoglycosides and the quinolones are e ff ective, but some cephalosporins and penicillin ma y not be. Many of  the carbapenems (e.g. mero - penem) are useful in severe infections. Bacteroides Bacteroides are non-spore-bearing, strict anaerobes that colonise the large bowel, vagina and oropharynx. Bacteroides fragilis is the principal organism that acts in synergy with aerobic Gram- - negative bacilli to cause SSIs, including intra-abdominal causes abscesses after colorectal or gynaecological surgery . They are sensitive to the imidazoles (e.g. metronidazole) and some - cephalosporins (e.g. cefotaxime). 

Clostridium tetani
(drumstick spores).

MICROBIOLOGY OF SURGICAL INFECTION Common bacteria involved in surgical infections

Streptococci Streptococci form chains and are Gram positive on staining ( Figure 5.2a ). The most important is the β -haemolytic Streptococcus , which resides in the pharynx of  5–10% of  the Figure 5.2 (a) (b) Rebecca Graighill Lancefield , 1895–1981, American bacteriologist, classified streptococci in 1933. - sification, it is the group A Streptococcus, also called Streptococcus pyogenes, that is the most pathogenic. It has the ability to spread, causing cellulitis, and to cause tissue destruction through the ). release of enzymes such as streptolysin, streptokinase and streptodornase. Streptococcus faecalis is an enterococcus in Lancefield group D. It is often found in synergy with other organisms, as are the γ -haemolytic Streptococcus and Peptostreptococcus , which is an anaerobe. Both Streptococcus pyogenes and Streptococcus faecalis may be involved in wound infection after bowel surgery , but the α -haemolytic Streptococcus viridans is not associated with wound infections. All the streptococci remain sensitive to penicillin and erythromycin. The cephalosporins are a suitable alternative in patients who are allergic to penicillin. Staphylococci Staphylococci form clumps and are Gram positive ( Figure 5.2b ). Staphylococcus aureus is the most important pathogen in - this group and is found in the nasopharynx of  up to 15% of  the population. It can cause suppuration in wounds and around implanted prostheses. Some strains are resistant to many common antibiotics (especially MRSA) and so are di ffi cult to treat. MRSA can be found in the nose of asymptomatic carriers among both patients and hospital workers, a potential source of infection after surgery . In parts of northern Europe, the prevalence of MRSA infections has been kept at very low levels using ‘search and destroy’ methods, which use screening techniques to look for MRSA in patients before they come in to hospital for elective surgery so that any carriers can be treated before their admission for surgery . Local policies on the management of  MRSA depend on the prevalence of  MRSA, the type of hospital, the clinical specialty and the availability of  facilities. Widespread swabbing, ward closures, isolation of patients and disinfection of  wards by deep cleaning must all be carefully considered. 

(a)
Streptococci.
Staphylococcal pus.
(b)

Figure 5.3 Staphylococcal infections are usually suppurative and localised. Most hospital Staphylococcus aureus strains are now β -lactamase producers and so are resistant to penicillin, but many strains remain sensitive to flucloxacillin, vancomycin, aminoglycosides and some cephalosporins. Nowadays, sev eral novel and innovative antibiotics have become available that have high activity against resistant strains. Some have the advantage of  good oral activity (linezolid), some have a wide spectrum (teicoplanin), some have good activity in bacteraemia (daptomy cin) but all are relatively expensive, and some have side e ff ects involving marrow , hepatic and renal toxicity . Their use is justified but needs to be controlled by tight local policies and guidelines that involve clinical microbiologists. Staphylococcus epidermidis (previously Staphylococcus albus also known as coagulase-negative Staphylococcus , was regarded as a non-pathogenic commensal organism commonly found on the skin, but is now recognised as a major threat in vascular and orthopaedic prosthetic surgery and in indwelling vascular cannulae/catheters. The bacteria form biofilms that adhere to prosthetic surfaces and limit the e ff ectiveness of  antibiotics. Clostridia Clostridial organisms are Gram-positive, obligate anaerobes that produce resistant spores ( Figure 5.3 ). Clostridium perfrin gens is the cause of  gas gangrene, and Clostridium tetani tetanus. Clostridium di ffi cile ( C. di ff . ) is the cause of  pseudomem branous colitis, in which destruction of  the normal colonic bacterial flora by antibiotic therapy allows an overgrowth of the normal gut commensal C. di ff . to pathological levels. Any antibiotic may cause this phenomenon, although the quino lones such as ciprofloxacin seem to be the highest risk, espe cially in elderly or immunocompromised patients. In its most severe form, the colitis may lead to perforation and the need for emergency colectomy with an associated high mortality . Treatment in volves resuscitation and antibiotic therapy . The fibrinous exudate is typical and di ff erentiates the colitis from other inflammatory diseases. Theodor Escherich, 1857–1911 , Professor of  Paediatrics, Vienna, Austria, discovered the Bacterium coli commune in 1886. Theodor Albrecht Edwin Klebs , 1834–1913, Professor of  Bacteriology successively at Prague, Czechoslovakia, Zurich, Switzerland and The Rush Medical College, Chicago, IL, USA. ing either C. di ff . glutamate dehydrogenase (GDH) antigen or C. di ff . toxin A/B. The Clostridium di ffi cile GDH Ag Rapid test qualitatively detects for the presence of C. di ff . GDH antigen in faeces. On the other hand, the Clostridium di ffi cile Toxin A/B rapid test qualitatively detects for the presence of C. di ff . toxins A and B in faeces. These rapid tests apply lateral flow immuno - chromatography and are for professional in vitro diagnostic use. Results are usually returned from this rapid testing in less than 30 minutes. Empirical treatment with metronidazole or vancomycin is recommended while awaiting results. Aerobic Gram-negative bacilli These bacilli are normal inhabitants of  the large bowel. Esch - erichia coli and Klebsiella spp. are lactose fermenting; Proteus is non-lactose fermenting. Most organisms in this group act in synergy with Bacteroides to cause SSIs after bowel operations (in particular, appendicitis, diverticulitis and peritonitis). Esch - erichia coli is a major cause of  urinary tract infection, although most aerobic Gram-negative bacilli can be involved, particu - larly in relation to urinary catheterisation. There is increasing concern about the development of  ESBLs in many of  this - group of  bacteria, which confer resistance to many antibiotics, particularly cephalosporins . Pseudomonas spp. tend to colonise burns and tracheostomy wounds, as well as the urinary tract. Once Pseudomonas has colonised wards and intensive care units (ICUs), it may be dif - ficult to eradicate. Surveillance of cross-infection is important in outbreaks. Hospital strains become resistant to β -lactamase as resistance can be transferred by plasmids. Wound infec - tions need antibiotic therapy only when there is prog ressive or ), spreading infection with systemic signs. The aminoglycosides and the quinolones are e ff ective, but some cephalosporins and penicillin ma y not be. Many of  the carbapenems (e.g. mero - penem) are useful in severe infections. Bacteroides Bacteroides are non-spore-bearing, strict anaerobes that colonise the large bowel, vagina and oropharynx. Bacteroides fragilis is the principal organism that acts in synergy with aerobic Gram- - negative bacilli to cause SSIs, including intra-abdominal causes abscesses after colorectal or gynaecological surgery . They are sensitive to the imidazoles (e.g. metronidazole) and some - cephalosporins (e.g. cefotaxime). 

Clostridium tetani
(drumstick spores).

# Misuse of antibiotic therapy with the risk of resi

Misuse of antibiotic therapy with the risk of resistance

Many staphylococci today have become resistant to penicillin. Often bacteria develop resistance through the acquisition of β -lactamases, which break up the β -lactam ring present in the molecular structure of  many antibiotics. The acquisition of  extended-spectrum β -lactamases (ESBLs) is an increasing concern in some Gram-negative organisms that cause urinary tract infections because it is di ffi cult to find an antibiotic y e ff ective against them. In addition, there is increasing concern about the rising resistance of  many other bacteria to anti - - biotics, in particular the emergence of  methicillin-resistant Staphylococcus aureus (MRSA), which is very relevant in general surgical practice. The introduction of  antibiotics for prophylaxis and for treatment, together with advances in anaesthesia and critical care medicine, has made possible surgery that would not pre - viously have been consider ed. Faecal peritonitis is no longer inevitably fatal, and incisions made in the presence of  such contamination can heal primarily without infection in over 90% of  patients with appropriate antibiotic therapy . Despite Penicillium notatum in 1928. 

(b)

closure in patients in whom the wound is known to be contam inated or dirty . Waiting for the wound to granulate and then performing a delayed primary or secondary closure may be considered a better option in such cases ( Summary box 5.2 Summary box 5.2 Advances in the control of infection in surgery /uni25CF /uni25CF /uni25CF SSI in patients who have contaminated wounds, who are immunosuppressed or who are undergoing prosthetic surgery is now the exception rather than the rule since the introduc tion of  prophylactic antibiotics. The evidence for this is of the highest level. The use of  prophylactic antibiotics in clean, non-prosthetic surgery is of  less value as infection rates are low and the indiscriminate use of  antibiotics simply encourages the emergence of resistant strains of  bacteria. 

Aseptic operating theatre techniques have enhanced the use of
antiseptics
Antibiotics have reduced postoperative infection rates after
elective and emergency surgery
Delayed primary, or secondary, closure remains useful in
heavily contaminated wounds

Misuse of antibiotic therapy with the risk of resistance

Many staphylococci today have become resistant to penicillin. Often bacteria develop resistance through the acquisition of β -lactamases, which break up the β -lactam ring present in the molecular structure of  many antibiotics. The acquisition of  extended-spectrum β -lactamases (ESBLs) is an increasing concern in some Gram-negative organisms that cause urinary tract infections because it is di ffi cult to find an antibiotic y e ff ective against them. In addition, there is increasing concern about the rising resistance of  many other bacteria to anti - - biotics, in particular the emergence of  methicillin-resistant Staphylococcus aureus (MRSA), which is very relevant in general surgical practice. The introduction of  antibiotics for prophylaxis and for treatment, together with advances in anaesthesia and critical care medicine, has made possible surgery that would not pre - viously have been consider ed. Faecal peritonitis is no longer inevitably fatal, and incisions made in the presence of  such contamination can heal primarily without infection in over 90% of  patients with appropriate antibiotic therapy . Despite Penicillium notatum in 1928. 

(b)

closure in patients in whom the wound is known to be contam inated or dirty . Waiting for the wound to granulate and then performing a delayed primary or secondary closure may be considered a better option in such cases ( Summary box 5.2 Summary box 5.2 Advances in the control of infection in surgery /uni25CF /uni25CF /uni25CF SSI in patients who have contaminated wounds, who are immunosuppressed or who are undergoing prosthetic surgery is now the exception rather than the rule since the introduc tion of  prophylactic antibiotics. The evidence for this is of the highest level. The use of  prophylactic antibiotics in clean, non-prosthetic surgery is of  less value as infection rates are low and the indiscriminate use of  antibiotics simply encourages the emergence of resistant strains of  bacteria. 

Aseptic operating theatre techniques have enhanced the use of
antiseptics
Antibiotics have reduced postoperative infection rates after
elective and emergency surgery
Delayed primary, or secondary, closure remains useful in
heavily contaminated wounds

# Misuse of antibiotic therapy with the risk of resistance

Misuse of antibiotic therapy with the risk of resistance

Many staphylococci today have become resistant to penicillin. Often bacteria develop resistance through the acquisition of β -lactamases, which break up the β -lactam ring present in the molecular structure of  many antibiotics. The acquisition of  extended-spectrum β -lactamases (ESBLs) is an increasing concern in some Gram-negative organisms that cause urinary tract infections because it is di ffi cult to find an antibiotic y e ff ective against them. In addition, there is increasing concern about the rising resistance of  many other bacteria to anti - - biotics, in particular the emergence of  methicillin-resistant Staphylococcus aureus (MRSA), which is very relevant in general surgical practice. The introduction of  antibiotics for prophylaxis and for treatment, together with advances in anaesthesia and critical care medicine, has made possible surgery that would not pre - viously have been consider ed. Faecal peritonitis is no longer inevitably fatal, and incisions made in the presence of  such contamination can heal primarily without infection in over 90% of  patients with appropriate antibiotic therapy . Despite Penicillium notatum in 1928. 

(b)

closure in patients in whom the wound is known to be contam inated or dirty . Waiting for the wound to granulate and then performing a delayed primary or secondary closure may be considered a better option in such cases ( Summary box 5.2 Summary box 5.2 Advances in the control of infection in surgery /uni25CF /uni25CF /uni25CF SSI in patients who have contaminated wounds, who are immunosuppressed or who are undergoing prosthetic surgery is now the exception rather than the rule since the introduc tion of  prophylactic antibiotics. The evidence for this is of the highest level. The use of  prophylactic antibiotics in clean, non-prosthetic surgery is of  less value as infection rates are low and the indiscriminate use of  antibiotics simply encourages the emergence of resistant strains of  bacteria. 

Aseptic operating theatre techniques have enhanced the use of
antiseptics
Antibiotics have reduced postoperative infection rates after
elective and emergency surgery
Delayed primary, or secondary, closure remains useful in
heavily contaminated wounds

# PRESENTATION OF SURGICAL INFECTION Major and minor surgical site infection (SSI)

PRESENTATION OF SURGICAL INFECTION Major and minor surgical site infection (SSI)

Infection acquired from the environment or the sta ff following surgery or admission to hospital is termed hospital-acquired infection (HAI). There are four main groups: respiratory infections (including ventilator-associated pneumonia), urinary tract infections (mostly related to urinary catheters), Figure 5.6 bacteraemia (mostly related to indwelling vascular catheters) and SSIs. A major SSI is defined as a wound that either discharges significant quantities of  pus spontaneously or needs a second - ary procedure to drain it ( Figure 5.4 ) . The patient may have systemic signs such as tachycardia, pyrexia and a raised white cell count ( Summary box 5.6 ). Summary box 5.6 Major wound infections /uni25CF /uni25CF /uni25CF Minor wound infections may discharge pus or infected - serous fluid but are not associated with excessive discomfort, of systemic signs or delay in return home ( Figure 5.7 ) . - Figure 5.7 

release
SIRS
IL-6, TNF , etc.
Release of
endotoxin
Macrophage
Colonisation by
Mesenteric
aerobic gram-
nodes
negative bacilli
(in gut failure
Translocation
and starvation)
(failure of gut-associated
lymphoid tissue,
villous atrophy)
Gut failure, colonisation and translocation related to the
development of systemic in
/f_l
ammatory response syndrome (SIRS)
and multiple organ dysfunction syndrome (MODS). IL, interleukin;
TNF , tumour necrosis factor.
Signi
/f_i
cant quantity of pus
Delayed return home
Patients are systemically ill
Minor wound infection that settled spontaneously without
antibiotics.

Abscess An abscess presents all the clinical features of  acute inflamma tion originally described by Celsus: calor (heat), rubor (redness), dolor (pain) and tumor (swelling). To these can be added laesa (loss of  function: if  it hurts, the infected part is not used). Abscesses usually follow a puncture wound of  some kind, which may have been forgotten, as well as surgery , but can be metastatic in all tissues following bacteraemia. Pyogenic organisms, predominantly Staphylococcus aureus, cause tissue necrosis and suppuration. Pus is composed of  dead and dying white blood cells, predominantly neutrophils, that have succumbed to bacterial toxins. An abscess is surrounded by an acute inflammatory response composed of  a fibrinous exudate, oedema and the cells of  acute inflammation. Gran ulation tissue (macrophages, fibroblasts and new blood vessel proliferation) forms later around the suppurative process and leads to collagen deposition. If  it is not drained or resorbed completely , a chronic abscess may result. If it is partly sterilised with empirical antibiotics, an antibioma may form. Abscesses contain hyperosmolar material that draws in fluid. This increases the pressure and causes pain. If they spread, they usually track along planes of least resistance and point towards the skin. Wound abscesses may discharge spontaneously by tracking to a surface but may need drainage through a surgical incision. Most abscesses relating to surgical wounds take 7–10 days to form after surgery . As many as 75% of  SSIs present after the patient has left hospital and may thus be overlooked by the surgical team. Abscess cavities need cleaning out after incision and drain age and are traditionally encouraged to heal by secondary intention. When the cavity is left open to drain freely , there is no need for antibiotic therapy as well. Antibiotics should be used if  the abscess cavity is closed after drainage, but the cavity should not be closed if  there is any risk of  retained loculi or f oreign material. Thus a perianal abscess can be incised and drained, the walls curetted and the skin closed with good results using appropriate antibiotic therapy , but a pilonidal abscess has a higher recurrence risk after such treatment because a nidus of hair may remain in the subcutaneous tissue adjacent to the abscess. Some small breast abscesses can be managed by simple needle aspiration of  the pus and antibiotic therapy ( Summary box 5.7 ). Persistent chronic abscesses may lead to sinus or fistula for mation. In a chronic abscess, lymphocytes and plasma cells are seen. There is tissue sequestration and later calcification may occur. Certain organisms are associated with chronicity and Mycobacte with sinus and fistula formation. Common ones are rium and Actinomyces. They should not be forgotten when these complications occur and persist. Perianastomotic contamination may be the cause of  an abscess but, in the abdomen, abscesses are more usually the result of anastomotic leakage. An abscess in a deep cavity suc as the pleura or peritoneum may be di ffi cult to diagnose or locate even when there is strong clinical suspicion that it is Aulus Aurelius Cornelius Celsus , 25 /uni00A0/b.sc/c.sc/e.sc –50 /uni00A0/c.sc/e.sc , Roman surgeon and the author of Abscesses - /uni25CF /uni25CF functio /uni25CF /uni25CF present ( Figure 5.8 ). Plain or contrast radiographs may not be helpful, but ultrasonography , computed tomography (CT), magnetic resonance imaging (MRI) and isotope-labelled white - cell scans are all useful and may allow image-guided aspiration and drainage of  intra-abdominal abscesses without the need for surgical intervention. Cellulitis and lymphangitis Cellulitis is a non-suppurative, invasive infection of  tissues, which is usually related to the point of  injury . There is poor localisation in addition to the cardinal signs of  spreading inflammation. Such infections presenting in surgical practice are typically caused by organisms such as β -haemolytic strepto - cocci ( Figure 5.9 ) , staphylococci ( Figure 5.10 ) and Clostridium perfringens. Tissue destruction, gangrene and ulceration may follow , which are caused by release of  proteases. - - - Figure 5.8 h De Re Medico Libri Octo. 

Abscesses need drainage
Modern imaging techniques may allow guided needle
aspiration, e.g. ultrasound-guided drainage of breast
abscesses
Antibiotics are indicated if the abscess cavity is not left open to
drain freely
An open abscess cavity heals by secondary intention
Plain radiograph showing a subphrenic abscess with a
gas/
/f_l
uid level (white arrow). Gastrogra
/f_i
n is seen leaking from the
oesophagojejunal anastomosis (after gastrectomy) towards the
abscess (black arrow).

Figure 5.9 Figure 5.10 Systemic signs (the old-fashioned term is toxaemia) are common, with chills, fever and rigors. These events follow the release of  toxins into the circulation, which stimulate a cytokine-mediated systemic inflammatory response even though blood cultures may be negative. Lymphangitis is part of  a similar process and presents as painful red streaks in a ff ected lymphatics draining the source of  infection. Lymphangitis is often accompanied by painful lymph node groups in the related drainage area, e.g. cervical, axillary or inguinal ( Summary box 5.8 ). Summary box 5.8 Cellulitis and lymphangitis /uni25CF /uni25CF /uni25CF Gas gangrene Gas gangrene is caused by Clostridium perfringens . These Gram-positive, anaerobic, spore-bearing bacilli are widely found in nature, particularly in soil and faeces. Patients who are immunocompromised, diabetic or have malignant disease are at greater risk, particularly if  they have wounds containing necrotic or foreign material, resulting in anaerobic conditions. Military wounds provide an ideal environment as the kinetic energy of  high-velocity missiles or shrapnel causes extensive tissue damage. The cavitation which follows passage of  a missile through the tissues causes a ‘sucking’ entry wound, leaving clothing and environmental soiling in the wound in addition to devascularised tissue. Gas gangrene wound infections are associated with severe local wound pain and crepitus (gas in the tissues, which may also be visible on plain radiographs). The wound produces a thin, brown, sweet-smelling exudate, in which Gram staining will reveal bacteria. Oedema and spread - ing gangrene follow the release of collagenase, hyaluronidase, other proteases and alpha toxin. Early systemic complications with circulatory collapse and organ failure follow if  prompt action is not taken ( Summary box 5.9 ). Antibiotic pr ophylaxis should always be considered in patients at risk, especially when amputations are performed for peripheral vascular disease with open necrotic ulceration. Once gas gangrene infection is established, large doses of intra venous penicillin and aggressive debridement of  a ff ected tissues are required. Summary box 5.9 Gas gangrene /uni25CF /uni25CF /uni25CF /uni25CF Clostridium tetani This is another anaerobic, terminal spore-bearing, Gram- positive bacterium, which can cause tetanus following implan - tation into tissues or a wound. The spores are widespread in soil and manure. The signs and symptoms of  tetanus are mediated by the release of  the exotoxin tetanospasmin; these include spasms in the distribution of  the short motor nerves of the face followed by the development of  severe generalised motor spasms including opisthotonus, respiratory arrest and death. Prophylaxis with tetanus toxoid is the best preventative treatment but, in an established infection, minor debridement of the wound may need to be performed and antibiotic treatment with benzylpenicillin provided in addition. Relaxants may also be required and the patient will require ventilation in severe forms, which are associated with a high mortality . 

Streptococcal cellulitis of the leg following a minor punc
ture wound.
Staphylococcal cellulitis of the face and orbit following
severe infection of an epidermoid cyst of the scalp.
Non-suppurative, poorly localised
Commonly caused by streptococci, staphylococci or clostridia
Blood cultures are often negative
-
Caused by
Clostridium perfringens
Gas and smell are characteristic
Immunocompromised patients are most at risk
Antibiotic prophylaxis is essential when performing
amputations to remove dead tissue

gangrene, necrotising fasciitis) This is a rare but serious bacterial infection that a ff ects and spreads via the deep fascia; hence, it is termed fasciitis. A mixed pattern of  organisms is responsible for this serious condition: coliforms, staphylococci, Bacteroides spp., anaerobic streptococci and peptostreptococci have all been implicated, acting in synergy . Often, aerobic bacteria destroy the living tissue, allowing anaerobic bacteria to thrive. Severe wound pain, signs of  spreading inflammation with crepitus and odour are all signs of  the infection spreading. Untreated, it will lead to widespread local gangrene and systemic multisystem organ failure. Abdominal wall infections are known as Meleney’s synergistic gangrene and scrotal infections as Fournier’s gangrene ( Figure 5.11 ). Patients are almost always immuno compromised, with conditions such as diabetes mellitus. The wound initiating the infection may have been minor, but severely contaminated wounds are more likely to be the cause. The subdermal spr ead of  gangrene is always much more extensive than appears from initial examination. The finger test can be used in the diagnosis of  patients who present with suspected necrotising fasciitis. The area of  suspected inv olvement is first infiltrated with local anaesthesia. A 2-cm incision is made in the skin down to the deep fascia. Lack of bleeding is a sign of necrotising fasciitis. On some occasions, a dishwater-coloured fluid is noticed seeping from the wound. Figure 5.11 Frank Lamont Meleney , 1889–1963, Professor of  Clinical Surgery , Columbia University , New Y ork, NY , USA. Jean Alfred Fournier , 1832–1915, syphilologist, the founder of  the V enereal and Dermatological Clinic, Hôpital Saint-Louis, Paris, France. by a sterile glove is then performed at the level of  the deep fascia. If  the tissues dissect with minimal resistance, the finger test is positive. Tissue biopsies are then sent for frozen section analysis. The characteristic histological findings are obliterative vasculitis of  the subcutaneous vessels, acute inflammation and subcutaneous tissue necrosis. If  either the finger test or rapid frozen section analysis is positive, or if the patient has progressive clinical findings consistent with necrotising fasciitis, immediate operative treatment must be initiated. Broad-spectrum antibiotic therapy must be combined with aggressive circulatory support. Locally , there should be wide otic tissue and laying open of  a ff ected areas. excision of necr The debridement may need to be extensive, and patients who survive may need large areas of  skin grafting later. - 

A classic presentation of Fournier’s gangrene of the
scrotum with ‘shameful exposure of the testes’ following excision of
the gangrenous skin.

# PRESENTATION OF SURGICAL INFECTION Major and minor

PRESENTATION OF SURGICAL INFECTION Major and minor surgical site infection (SSI)

Infection acquired from the environment or the sta ff following surgery or admission to hospital is termed hospital-acquired infection (HAI). There are four main groups: respiratory infections (including ventilator-associated pneumonia), urinary tract infections (mostly related to urinary catheters), Figure 5.6 bacteraemia (mostly related to indwelling vascular catheters) and SSIs. A major SSI is defined as a wound that either discharges significant quantities of  pus spontaneously or needs a second - ary procedure to drain it ( Figure 5.4 ) . The patient may have systemic signs such as tachycardia, pyrexia and a raised white cell count ( Summary box 5.6 ). Summary box 5.6 Major wound infections /uni25CF /uni25CF /uni25CF Minor wound infections may discharge pus or infected - serous fluid but are not associated with excessive discomfort, of systemic signs or delay in return home ( Figure 5.7 ) . - Figure 5.7 

release
SIRS
IL-6, TNF , etc.
Release of
endotoxin
Macrophage
Colonisation by
Mesenteric
aerobic gram-
nodes
negative bacilli
(in gut failure
Translocation
and starvation)
(failure of gut-associated
lymphoid tissue,
villous atrophy)
Gut failure, colonisation and translocation related to the
development of systemic in
/f_l
ammatory response syndrome (SIRS)
and multiple organ dysfunction syndrome (MODS). IL, interleukin;
TNF , tumour necrosis factor.
Signi
/f_i
cant quantity of pus
Delayed return home
Patients are systemically ill
Minor wound infection that settled spontaneously without
antibiotics.

Abscess An abscess presents all the clinical features of  acute inflamma tion originally described by Celsus: calor (heat), rubor (redness), dolor (pain) and tumor (swelling). To these can be added laesa (loss of  function: if  it hurts, the infected part is not used). Abscesses usually follow a puncture wound of  some kind, which may have been forgotten, as well as surgery , but can be metastatic in all tissues following bacteraemia. Pyogenic organisms, predominantly Staphylococcus aureus, cause tissue necrosis and suppuration. Pus is composed of  dead and dying white blood cells, predominantly neutrophils, that have succumbed to bacterial toxins. An abscess is surrounded by an acute inflammatory response composed of  a fibrinous exudate, oedema and the cells of  acute inflammation. Gran ulation tissue (macrophages, fibroblasts and new blood vessel proliferation) forms later around the suppurative process and leads to collagen deposition. If  it is not drained or resorbed completely , a chronic abscess may result. If it is partly sterilised with empirical antibiotics, an antibioma may form. Abscesses contain hyperosmolar material that draws in fluid. This increases the pressure and causes pain. If they spread, they usually track along planes of least resistance and point towards the skin. Wound abscesses may discharge spontaneously by tracking to a surface but may need drainage through a surgical incision. Most abscesses relating to surgical wounds take 7–10 days to form after surgery . As many as 75% of  SSIs present after the patient has left hospital and may thus be overlooked by the surgical team. Abscess cavities need cleaning out after incision and drain age and are traditionally encouraged to heal by secondary intention. When the cavity is left open to drain freely , there is no need for antibiotic therapy as well. Antibiotics should be used if  the abscess cavity is closed after drainage, but the cavity should not be closed if  there is any risk of  retained loculi or f oreign material. Thus a perianal abscess can be incised and drained, the walls curetted and the skin closed with good results using appropriate antibiotic therapy , but a pilonidal abscess has a higher recurrence risk after such treatment because a nidus of hair may remain in the subcutaneous tissue adjacent to the abscess. Some small breast abscesses can be managed by simple needle aspiration of  the pus and antibiotic therapy ( Summary box 5.7 ). Persistent chronic abscesses may lead to sinus or fistula for mation. In a chronic abscess, lymphocytes and plasma cells are seen. There is tissue sequestration and later calcification may occur. Certain organisms are associated with chronicity and Mycobacte with sinus and fistula formation. Common ones are rium and Actinomyces. They should not be forgotten when these complications occur and persist. Perianastomotic contamination may be the cause of  an abscess but, in the abdomen, abscesses are more usually the result of anastomotic leakage. An abscess in a deep cavity suc as the pleura or peritoneum may be di ffi cult to diagnose or locate even when there is strong clinical suspicion that it is Aulus Aurelius Cornelius Celsus , 25 /uni00A0/b.sc/c.sc/e.sc –50 /uni00A0/c.sc/e.sc , Roman surgeon and the author of Abscesses - /uni25CF /uni25CF functio /uni25CF /uni25CF present ( Figure 5.8 ). Plain or contrast radiographs may not be helpful, but ultrasonography , computed tomography (CT), magnetic resonance imaging (MRI) and isotope-labelled white - cell scans are all useful and may allow image-guided aspiration and drainage of  intra-abdominal abscesses without the need for surgical intervention. Cellulitis and lymphangitis Cellulitis is a non-suppurative, invasive infection of  tissues, which is usually related to the point of  injury . There is poor localisation in addition to the cardinal signs of  spreading inflammation. Such infections presenting in surgical practice are typically caused by organisms such as β -haemolytic strepto - cocci ( Figure 5.9 ) , staphylococci ( Figure 5.10 ) and Clostridium perfringens. Tissue destruction, gangrene and ulceration may follow , which are caused by release of  proteases. - - - Figure 5.8 h De Re Medico Libri Octo. 

Abscesses need drainage
Modern imaging techniques may allow guided needle
aspiration, e.g. ultrasound-guided drainage of breast
abscesses
Antibiotics are indicated if the abscess cavity is not left open to
drain freely
An open abscess cavity heals by secondary intention
Plain radiograph showing a subphrenic abscess with a
gas/
/f_l
uid level (white arrow). Gastrogra
/f_i
n is seen leaking from the
oesophagojejunal anastomosis (after gastrectomy) towards the
abscess (black arrow).

Figure 5.9 Figure 5.10 Systemic signs (the old-fashioned term is toxaemia) are common, with chills, fever and rigors. These events follow the release of  toxins into the circulation, which stimulate a cytokine-mediated systemic inflammatory response even though blood cultures may be negative. Lymphangitis is part of  a similar process and presents as painful red streaks in a ff ected lymphatics draining the source of  infection. Lymphangitis is often accompanied by painful lymph node groups in the related drainage area, e.g. cervical, axillary or inguinal ( Summary box 5.8 ). Summary box 5.8 Cellulitis and lymphangitis /uni25CF /uni25CF /uni25CF Gas gangrene Gas gangrene is caused by Clostridium perfringens . These Gram-positive, anaerobic, spore-bearing bacilli are widely found in nature, particularly in soil and faeces. Patients who are immunocompromised, diabetic or have malignant disease are at greater risk, particularly if  they have wounds containing necrotic or foreign material, resulting in anaerobic conditions. Military wounds provide an ideal environment as the kinetic energy of  high-velocity missiles or shrapnel causes extensive tissue damage. The cavitation which follows passage of  a missile through the tissues causes a ‘sucking’ entry wound, leaving clothing and environmental soiling in the wound in addition to devascularised tissue. Gas gangrene wound infections are associated with severe local wound pain and crepitus (gas in the tissues, which may also be visible on plain radiographs). The wound produces a thin, brown, sweet-smelling exudate, in which Gram staining will reveal bacteria. Oedema and spread - ing gangrene follow the release of collagenase, hyaluronidase, other proteases and alpha toxin. Early systemic complications with circulatory collapse and organ failure follow if  prompt action is not taken ( Summary box 5.9 ). Antibiotic pr ophylaxis should always be considered in patients at risk, especially when amputations are performed for peripheral vascular disease with open necrotic ulceration. Once gas gangrene infection is established, large doses of intra venous penicillin and aggressive debridement of  a ff ected tissues are required. Summary box 5.9 Gas gangrene /uni25CF /uni25CF /uni25CF /uni25CF Clostridium tetani This is another anaerobic, terminal spore-bearing, Gram- positive bacterium, which can cause tetanus following implan - tation into tissues or a wound. The spores are widespread in soil and manure. The signs and symptoms of  tetanus are mediated by the release of  the exotoxin tetanospasmin; these include spasms in the distribution of  the short motor nerves of the face followed by the development of  severe generalised motor spasms including opisthotonus, respiratory arrest and death. Prophylaxis with tetanus toxoid is the best preventative treatment but, in an established infection, minor debridement of the wound may need to be performed and antibiotic treatment with benzylpenicillin provided in addition. Relaxants may also be required and the patient will require ventilation in severe forms, which are associated with a high mortality . 

Streptococcal cellulitis of the leg following a minor punc
ture wound.
Staphylococcal cellulitis of the face and orbit following
severe infection of an epidermoid cyst of the scalp.
Non-suppurative, poorly localised
Commonly caused by streptococci, staphylococci or clostridia
Blood cultures are often negative
-
Caused by
Clostridium perfringens
Gas and smell are characteristic
Immunocompromised patients are most at risk
Antibiotic prophylaxis is essential when performing
amputations to remove dead tissue

gangrene, necrotising fasciitis) This is a rare but serious bacterial infection that a ff ects and spreads via the deep fascia; hence, it is termed fasciitis. A mixed pattern of  organisms is responsible for this serious condition: coliforms, staphylococci, Bacteroides spp., anaerobic streptococci and peptostreptococci have all been implicated, acting in synergy . Often, aerobic bacteria destroy the living tissue, allowing anaerobic bacteria to thrive. Severe wound pain, signs of  spreading inflammation with crepitus and odour are all signs of  the infection spreading. Untreated, it will lead to widespread local gangrene and systemic multisystem organ failure. Abdominal wall infections are known as Meleney’s synergistic gangrene and scrotal infections as Fournier’s gangrene ( Figure 5.11 ). Patients are almost always immuno compromised, with conditions such as diabetes mellitus. The wound initiating the infection may have been minor, but severely contaminated wounds are more likely to be the cause. The subdermal spr ead of  gangrene is always much more extensive than appears from initial examination. The finger test can be used in the diagnosis of  patients who present with suspected necrotising fasciitis. The area of  suspected inv olvement is first infiltrated with local anaesthesia. A 2-cm incision is made in the skin down to the deep fascia. Lack of bleeding is a sign of necrotising fasciitis. On some occasions, a dishwater-coloured fluid is noticed seeping from the wound. Figure 5.11 Frank Lamont Meleney , 1889–1963, Professor of  Clinical Surgery , Columbia University , New Y ork, NY , USA. Jean Alfred Fournier , 1832–1915, syphilologist, the founder of  the V enereal and Dermatological Clinic, Hôpital Saint-Louis, Paris, France. by a sterile glove is then performed at the level of  the deep fascia. If  the tissues dissect with minimal resistance, the finger test is positive. Tissue biopsies are then sent for frozen section analysis. The characteristic histological findings are obliterative vasculitis of  the subcutaneous vessels, acute inflammation and subcutaneous tissue necrosis. If  either the finger test or rapid frozen section analysis is positive, or if the patient has progressive clinical findings consistent with necrotising fasciitis, immediate operative treatment must be initiated. Broad-spectrum antibiotic therapy must be combined with aggressive circulatory support. Locally , there should be wide otic tissue and laying open of  a ff ected areas. excision of necr The debridement may need to be extensive, and patients who survive may need large areas of  skin grafting later. - 

A classic presentation of Fournier’s gangrene of the
scrotum with ‘shameful exposure of the testes’ following excision of
the gangrenous skin.

PRESENTATION OF SURGICAL INFECTION Major and minor surgical site infection (SSI)

Infection acquired from the environment or the sta ff following surgery or admission to hospital is termed hospital-acquired infection (HAI). There are four main groups: respiratory infections (including ventilator-associated pneumonia), urinary tract infections (mostly related to urinary catheters), Figure 5.6 bacteraemia (mostly related to indwelling vascular catheters) and SSIs. A major SSI is defined as a wound that either discharges significant quantities of  pus spontaneously or needs a second - ary procedure to drain it ( Figure 5.4 ) . The patient may have systemic signs such as tachycardia, pyrexia and a raised white cell count ( Summary box 5.6 ). Summary box 5.6 Major wound infections /uni25CF /uni25CF /uni25CF Minor wound infections may discharge pus or infected - serous fluid but are not associated with excessive discomfort, of systemic signs or delay in return home ( Figure 5.7 ) . - Figure 5.7 

release
SIRS
IL-6, TNF , etc.
Release of
endotoxin
Macrophage
Colonisation by
Mesenteric
aerobic gram-
nodes
negative bacilli
(in gut failure
Translocation
and starvation)
(failure of gut-associated
lymphoid tissue,
villous atrophy)
Gut failure, colonisation and translocation related to the
development of systemic in
/f_l
ammatory response syndrome (SIRS)
and multiple organ dysfunction syndrome (MODS). IL, interleukin;
TNF , tumour necrosis factor.
Signi
/f_i
cant quantity of pus
Delayed return home
Patients are systemically ill
Minor wound infection that settled spontaneously without
antibiotics.

Abscess An abscess presents all the clinical features of  acute inflamma tion originally described by Celsus: calor (heat), rubor (redness), dolor (pain) and tumor (swelling). To these can be added laesa (loss of  function: if  it hurts, the infected part is not used). Abscesses usually follow a puncture wound of  some kind, which may have been forgotten, as well as surgery , but can be metastatic in all tissues following bacteraemia. Pyogenic organisms, predominantly Staphylococcus aureus, cause tissue necrosis and suppuration. Pus is composed of  dead and dying white blood cells, predominantly neutrophils, that have succumbed to bacterial toxins. An abscess is surrounded by an acute inflammatory response composed of  a fibrinous exudate, oedema and the cells of  acute inflammation. Gran ulation tissue (macrophages, fibroblasts and new blood vessel proliferation) forms later around the suppurative process and leads to collagen deposition. If  it is not drained or resorbed completely , a chronic abscess may result. If it is partly sterilised with empirical antibiotics, an antibioma may form. Abscesses contain hyperosmolar material that draws in fluid. This increases the pressure and causes pain. If they spread, they usually track along planes of least resistance and point towards the skin. Wound abscesses may discharge spontaneously by tracking to a surface but may need drainage through a surgical incision. Most abscesses relating to surgical wounds take 7–10 days to form after surgery . As many as 75% of  SSIs present after the patient has left hospital and may thus be overlooked by the surgical team. Abscess cavities need cleaning out after incision and drain age and are traditionally encouraged to heal by secondary intention. When the cavity is left open to drain freely , there is no need for antibiotic therapy as well. Antibiotics should be used if  the abscess cavity is closed after drainage, but the cavity should not be closed if  there is any risk of  retained loculi or f oreign material. Thus a perianal abscess can be incised and drained, the walls curetted and the skin closed with good results using appropriate antibiotic therapy , but a pilonidal abscess has a higher recurrence risk after such treatment because a nidus of hair may remain in the subcutaneous tissue adjacent to the abscess. Some small breast abscesses can be managed by simple needle aspiration of  the pus and antibiotic therapy ( Summary box 5.7 ). Persistent chronic abscesses may lead to sinus or fistula for mation. In a chronic abscess, lymphocytes and plasma cells are seen. There is tissue sequestration and later calcification may occur. Certain organisms are associated with chronicity and Mycobacte with sinus and fistula formation. Common ones are rium and Actinomyces. They should not be forgotten when these complications occur and persist. Perianastomotic contamination may be the cause of  an abscess but, in the abdomen, abscesses are more usually the result of anastomotic leakage. An abscess in a deep cavity suc as the pleura or peritoneum may be di ffi cult to diagnose or locate even when there is strong clinical suspicion that it is Aulus Aurelius Cornelius Celsus , 25 /uni00A0/b.sc/c.sc/e.sc –50 /uni00A0/c.sc/e.sc , Roman surgeon and the author of Abscesses - /uni25CF /uni25CF functio /uni25CF /uni25CF present ( Figure 5.8 ). Plain or contrast radiographs may not be helpful, but ultrasonography , computed tomography (CT), magnetic resonance imaging (MRI) and isotope-labelled white - cell scans are all useful and may allow image-guided aspiration and drainage of  intra-abdominal abscesses without the need for surgical intervention. Cellulitis and lymphangitis Cellulitis is a non-suppurative, invasive infection of  tissues, which is usually related to the point of  injury . There is poor localisation in addition to the cardinal signs of  spreading inflammation. Such infections presenting in surgical practice are typically caused by organisms such as β -haemolytic strepto - cocci ( Figure 5.9 ) , staphylococci ( Figure 5.10 ) and Clostridium perfringens. Tissue destruction, gangrene and ulceration may follow , which are caused by release of  proteases. - - - Figure 5.8 h De Re Medico Libri Octo. 

Abscesses need drainage
Modern imaging techniques may allow guided needle
aspiration, e.g. ultrasound-guided drainage of breast
abscesses
Antibiotics are indicated if the abscess cavity is not left open to
drain freely
An open abscess cavity heals by secondary intention
Plain radiograph showing a subphrenic abscess with a
gas/
/f_l
uid level (white arrow). Gastrogra
/f_i
n is seen leaking from the
oesophagojejunal anastomosis (after gastrectomy) towards the
abscess (black arrow).

Figure 5.9 Figure 5.10 Systemic signs (the old-fashioned term is toxaemia) are common, with chills, fever and rigors. These events follow the release of  toxins into the circulation, which stimulate a cytokine-mediated systemic inflammatory response even though blood cultures may be negative. Lymphangitis is part of  a similar process and presents as painful red streaks in a ff ected lymphatics draining the source of  infection. Lymphangitis is often accompanied by painful lymph node groups in the related drainage area, e.g. cervical, axillary or inguinal ( Summary box 5.8 ). Summary box 5.8 Cellulitis and lymphangitis /uni25CF /uni25CF /uni25CF Gas gangrene Gas gangrene is caused by Clostridium perfringens . These Gram-positive, anaerobic, spore-bearing bacilli are widely found in nature, particularly in soil and faeces. Patients who are immunocompromised, diabetic or have malignant disease are at greater risk, particularly if  they have wounds containing necrotic or foreign material, resulting in anaerobic conditions. Military wounds provide an ideal environment as the kinetic energy of  high-velocity missiles or shrapnel causes extensive tissue damage. The cavitation which follows passage of  a missile through the tissues causes a ‘sucking’ entry wound, leaving clothing and environmental soiling in the wound in addition to devascularised tissue. Gas gangrene wound infections are associated with severe local wound pain and crepitus (gas in the tissues, which may also be visible on plain radiographs). The wound produces a thin, brown, sweet-smelling exudate, in which Gram staining will reveal bacteria. Oedema and spread - ing gangrene follow the release of collagenase, hyaluronidase, other proteases and alpha toxin. Early systemic complications with circulatory collapse and organ failure follow if  prompt action is not taken ( Summary box 5.9 ). Antibiotic pr ophylaxis should always be considered in patients at risk, especially when amputations are performed for peripheral vascular disease with open necrotic ulceration. Once gas gangrene infection is established, large doses of intra venous penicillin and aggressive debridement of  a ff ected tissues are required. Summary box 5.9 Gas gangrene /uni25CF /uni25CF /uni25CF /uni25CF Clostridium tetani This is another anaerobic, terminal spore-bearing, Gram- positive bacterium, which can cause tetanus following implan - tation into tissues or a wound. The spores are widespread in soil and manure. The signs and symptoms of  tetanus are mediated by the release of  the exotoxin tetanospasmin; these include spasms in the distribution of  the short motor nerves of the face followed by the development of  severe generalised motor spasms including opisthotonus, respiratory arrest and death. Prophylaxis with tetanus toxoid is the best preventative treatment but, in an established infection, minor debridement of the wound may need to be performed and antibiotic treatment with benzylpenicillin provided in addition. Relaxants may also be required and the patient will require ventilation in severe forms, which are associated with a high mortality . 

Streptococcal cellulitis of the leg following a minor punc
ture wound.
Staphylococcal cellulitis of the face and orbit following
severe infection of an epidermoid cyst of the scalp.
Non-suppurative, poorly localised
Commonly caused by streptococci, staphylococci or clostridia
Blood cultures are often negative
-
Caused by
Clostridium perfringens
Gas and smell are characteristic
Immunocompromised patients are most at risk
Antibiotic prophylaxis is essential when performing
amputations to remove dead tissue

gangrene, necrotising fasciitis) This is a rare but serious bacterial infection that a ff ects and spreads via the deep fascia; hence, it is termed fasciitis. A mixed pattern of  organisms is responsible for this serious condition: coliforms, staphylococci, Bacteroides spp., anaerobic streptococci and peptostreptococci have all been implicated, acting in synergy . Often, aerobic bacteria destroy the living tissue, allowing anaerobic bacteria to thrive. Severe wound pain, signs of  spreading inflammation with crepitus and odour are all signs of  the infection spreading. Untreated, it will lead to widespread local gangrene and systemic multisystem organ failure. Abdominal wall infections are known as Meleney’s synergistic gangrene and scrotal infections as Fournier’s gangrene ( Figure 5.11 ). Patients are almost always immuno compromised, with conditions such as diabetes mellitus. The wound initiating the infection may have been minor, but severely contaminated wounds are more likely to be the cause. The subdermal spr ead of  gangrene is always much more extensive than appears from initial examination. The finger test can be used in the diagnosis of  patients who present with suspected necrotising fasciitis. The area of  suspected inv olvement is first infiltrated with local anaesthesia. A 2-cm incision is made in the skin down to the deep fascia. Lack of bleeding is a sign of necrotising fasciitis. On some occasions, a dishwater-coloured fluid is noticed seeping from the wound. Figure 5.11 Frank Lamont Meleney , 1889–1963, Professor of  Clinical Surgery , Columbia University , New Y ork, NY , USA. Jean Alfred Fournier , 1832–1915, syphilologist, the founder of  the V enereal and Dermatological Clinic, Hôpital Saint-Louis, Paris, France. by a sterile glove is then performed at the level of  the deep fascia. If  the tissues dissect with minimal resistance, the finger test is positive. Tissue biopsies are then sent for frozen section analysis. The characteristic histological findings are obliterative vasculitis of  the subcutaneous vessels, acute inflammation and subcutaneous tissue necrosis. If  either the finger test or rapid frozen section analysis is positive, or if the patient has progressive clinical findings consistent with necrotising fasciitis, immediate operative treatment must be initiated. Broad-spectrum antibiotic therapy must be combined with aggressive circulatory support. Locally , there should be wide otic tissue and laying open of  a ff ected areas. excision of necr The debridement may need to be extensive, and patients who survive may need large areas of  skin grafting later. - 

A classic presentation of Fournier’s gangrene of the
scrotum with ‘shameful exposure of the testes’ following excision of
the gangrenous skin.

# Postoperative wound infections

Postoperative wound infections

The majority of  wound infections arise from endogenous sources within the patient, but exogenous SSIs may also occur HOSPI TA L __________________________________ __ __ ____ ____ _ __ ____ __ ___________ DA DA TE OF BIR TE OF BIR TH TH UNIT NO UNIT NO YEAR WARD SURNAME SURNAME SEX SEX CONSUL CO CONSUL T T ANT ANT FIRST NAMES FIRST NAMES JJ
ff BOWELS: 0 0 0 0 MONTH AUGUST th th th th th th th DAY 6 7 8 9 10 11 12 5 0 0 0 HOURS 11 11 22 25 14 6 17 23 11 11 09 22 22 22 6 23 10 7 06 18 1 0 0 21 0 0 3 0 0 0 0 0 0 30 7 17 0 T MINUTES TIME 17 30 0 0 06 17 0 0 0 0 0 0 0 0 30 0 40.5 40.0 39.5 Fan therapy 39.0 Fan therapy 38.5 CELSIUS) ∞ 38.0 20-30 37.5 TURE ( 37.0 36.5 TEMPERA 36.0 35.5 35.0 170 34.5 160 34.0 150 140 130 120 PULSE PER MINUTE 110 100 90 80 70 60 50 40 TION PER MINUTE 30 20 RESPIRA 10 Figure 5.13 related to poor hospital standards. Strict attention to ward cleanliness, gloving before touching patient wounds and hand - washing between all patient contacts are important preventive measures. An outbreak of  wound infections on the ward with bacteria having the same antibiotic sensitivity profile implies an exogenous source of  infection, which needs to be investigated by swabbing all sta ff and work surfaces. It may need temporary ward closure and a deep clean to eradicate the infection source. Now that patients are discharged more quickly after sur - gery and many procedures are performed as day cases, many SSIs are missed by the surgical team unless they undertake a prolonged and carefully audited follow-up with primary care doctors. Suppurative wound infections take 7–10 days to elop, and even cellulitis around wounds caused by inva - dev sive organisms (such as β -haemolytic Streptococcus ) takes 3–4 days to develop. Major surgical infections with systemic signs ( Figure 5.13 ), evidence of spreading infection, cellulitis or bacteraemia need treatment with appropriate antibiotics. The choice may need to be empirical initially but is best based on culture and sensitivities of  isolates harvested at surgery or from e of  wound fluids or wound swabs. Although the iden - cultur tification of  organisms in surgical infections is necessary for audit and wound surveillance purposes, it is usually 2–3 days before sensitivities are known ( Figures 5.14 and 5.15 ) . It is illogical to withhold antibiotics until results are available but, if  clinical response is poor by the time sensitivities are known, then antibiotics can be changed. Such changes are unusual if choice of antibiotics is sensible; change of  anti - the empirical biotics promotes resistance and risks complications, such as C. di ff . enteritis. If  an infected wound is under tension, or there is clear evi - dence of  suppuration, sutures or clips need to be removed, with curettage if  necessary , to allow pus to drain adequately . In severely contaminated wounds, such as an incision made for drainage of  an abscess, it is logical to lea ve the skin open. Delayed primary or secondary closure can be undertaken when the wound is clean and granulating ( Figures 5.16 and 5.17 ) . 250 240 Some heavily infected wounds may be left to heal by secondary 230 intention, with no attempt at closure, particularly where there 220 210 is a loss of  skin cover and healthy granulation tissue develops 200 190 BLOOD PRESSURE mmHg 180 170 160 150 140 130 120 110 100 90 80 70 60 Figure 5.14 

Classic swinging pyrexia related to a perianastomotic
wound abscess that settled spontaneously on antibiotic therapy.
Mixed streptococcal infection of a skin graft with very
poor ‘take’.

Figure 5.15 Figure 5.14 (a) (b) Figure 5.16 (a, b) Figure 5.17 that can always be revised with plastic surgery under clean surgical conditions at a later stage ( Summary box 5.13 ). Summary box 5.13 Surgical incisions through infected or contaminated tissues /uni25CF /uni25CF /uni25CF When taking pus from infected wounds, specimens should be sent fresh for microbiological culture. Swabs should be placed in transport medium, but the larger the volume of  pus sent, the more likely is the accurate identification of  the organ - ism involved. Providing the microbiologist with as much infor - mation as possible and discussing the results with them gives the best chance of  the most appropriate antibiotic treatment. If bacteraemia is suspected, but results are nega tive, then repeat specimens for blood culture and an immediate Gram stain. Topical antiseptics should only be used on heavily con - taminated wounds for a short period to clear infection as they inhibit epithelial ingrowth and so impair wound healing. 

After 5–6 days of antibiotics, the infection shown in
is under control, and the skin grafts are clearly viable.
Delayed primary closure of a fasciotomy wound
after 3–5 days.
Skin layers left open to granulate after laparotomy for
faecal peritonitis, ready for skin grafting.
When possible, tissue or pus for culture should be taken before
antibiotic cover is started
The choice of antibiotics is empirical until sensitivities are
available
Heavily contaminated wounds are best managed by delayed
primary or secondary closure

Postoperative wound infections

The majority of  wound infections arise from endogenous sources within the patient, but exogenous SSIs may also occur HOSPI TA L __________________________________ __ __ ____ ____ _ __ ____ __ ___________ DA DA TE OF BIR TE OF BIR TH TH UNIT NO UNIT NO YEAR WARD SURNAME SURNAME SEX SEX CONSUL CO CONSUL T T ANT ANT FIRST NAMES FIRST NAMES JJ
ff BOWELS: 0 0 0 0 MONTH AUGUST th th th th th th th DAY 6 7 8 9 10 11 12 5 0 0 0 HOURS 11 11 22 25 14 6 17 23 11 11 09 22 22 22 6 23 10 7 06 18 1 0 0 21 0 0 3 0 0 0 0 0 0 30 7 17 0 T MINUTES TIME 17 30 0 0 06 17 0 0 0 0 0 0 0 0 30 0 40.5 40.0 39.5 Fan therapy 39.0 Fan therapy 38.5 CELSIUS) ∞ 38.0 20-30 37.5 TURE ( 37.0 36.5 TEMPERA 36.0 35.5 35.0 170 34.5 160 34.0 150 140 130 120 PULSE PER MINUTE 110 100 90 80 70 60 50 40 TION PER MINUTE 30 20 RESPIRA 10 Figure 5.13 related to poor hospital standards. Strict attention to ward cleanliness, gloving before touching patient wounds and hand - washing between all patient contacts are important preventive measures. An outbreak of  wound infections on the ward with bacteria having the same antibiotic sensitivity profile implies an exogenous source of  infection, which needs to be investigated by swabbing all sta ff and work surfaces. It may need temporary ward closure and a deep clean to eradicate the infection source. Now that patients are discharged more quickly after sur - gery and many procedures are performed as day cases, many SSIs are missed by the surgical team unless they undertake a prolonged and carefully audited follow-up with primary care doctors. Suppurative wound infections take 7–10 days to elop, and even cellulitis around wounds caused by inva - dev sive organisms (such as β -haemolytic Streptococcus ) takes 3–4 days to develop. Major surgical infections with systemic signs ( Figure 5.13 ), evidence of spreading infection, cellulitis or bacteraemia need treatment with appropriate antibiotics. The choice may need to be empirical initially but is best based on culture and sensitivities of  isolates harvested at surgery or from e of  wound fluids or wound swabs. Although the iden - cultur tification of  organisms in surgical infections is necessary for audit and wound surveillance purposes, it is usually 2–3 days before sensitivities are known ( Figures 5.14 and 5.15 ) . It is illogical to withhold antibiotics until results are available but, if  clinical response is poor by the time sensitivities are known, then antibiotics can be changed. Such changes are unusual if choice of antibiotics is sensible; change of  anti - the empirical biotics promotes resistance and risks complications, such as C. di ff . enteritis. If  an infected wound is under tension, or there is clear evi - dence of  suppuration, sutures or clips need to be removed, with curettage if  necessary , to allow pus to drain adequately . In severely contaminated wounds, such as an incision made for drainage of  an abscess, it is logical to lea ve the skin open. Delayed primary or secondary closure can be undertaken when the wound is clean and granulating ( Figures 5.16 and 5.17 ) . 250 240 Some heavily infected wounds may be left to heal by secondary 230 intention, with no attempt at closure, particularly where there 220 210 is a loss of  skin cover and healthy granulation tissue develops 200 190 BLOOD PRESSURE mmHg 180 170 160 150 140 130 120 110 100 90 80 70 60 Figure 5.14 

Classic swinging pyrexia related to a perianastomotic
wound abscess that settled spontaneously on antibiotic therapy.
Mixed streptococcal infection of a skin graft with very
poor ‘take’.

Figure 5.15 Figure 5.14 (a) (b) Figure 5.16 (a, b) Figure 5.17 that can always be revised with plastic surgery under clean surgical conditions at a later stage ( Summary box 5.13 ). Summary box 5.13 Surgical incisions through infected or contaminated tissues /uni25CF /uni25CF /uni25CF When taking pus from infected wounds, specimens should be sent fresh for microbiological culture. Swabs should be placed in transport medium, but the larger the volume of  pus sent, the more likely is the accurate identification of  the organ - ism involved. Providing the microbiologist with as much infor - mation as possible and discussing the results with them gives the best chance of  the most appropriate antibiotic treatment. If bacteraemia is suspected, but results are nega tive, then repeat specimens for blood culture and an immediate Gram stain. Topical antiseptics should only be used on heavily con - taminated wounds for a short period to clear infection as they inhibit epithelial ingrowth and so impair wound healing. 

After 5–6 days of antibiotics, the infection shown in
is under control, and the skin grafts are clearly viable.
Delayed primary closure of a fasciotomy wound
after 3–5 days.
Skin layers left open to granulate after laparotomy for
faecal peritonitis, ready for skin grafting.
When possible, tissue or pus for culture should be taken before
antibiotic cover is started
The choice of antibiotics is empirical until sensitivities are
available
Heavily contaminated wounds are best managed by delayed
primary or secondary closure

Postoperative wound infections

The majority of  wound infections arise from endogenous sources within the patient, but exogenous SSIs may also occur HOSPI TA L __________________________________ __ __ ____ ____ _ __ ____ __ ___________ DA DA TE OF BIR TE OF BIR TH TH UNIT NO UNIT NO YEAR WARD SURNAME SURNAME SEX SEX CONSUL CO CONSUL T T ANT ANT FIRST NAMES FIRST NAMES JJ
ff BOWELS: 0 0 0 0 MONTH AUGUST th th th th th th th DAY 6 7 8 9 10 11 12 5 0 0 0 HOURS 11 11 22 25 14 6 17 23 11 11 09 22 22 22 6 23 10 7 06 18 1 0 0 21 0 0 3 0 0 0 0 0 0 30 7 17 0 T MINUTES TIME 17 30 0 0 06 17 0 0 0 0 0 0 0 0 30 0 40.5 40.0 39.5 Fan therapy 39.0 Fan therapy 38.5 CELSIUS) ∞ 38.0 20-30 37.5 TURE ( 37.0 36.5 TEMPERA 36.0 35.5 35.0 170 34.5 160 34.0 150 140 130 120 PULSE PER MINUTE 110 100 90 80 70 60 50 40 TION PER MINUTE 30 20 RESPIRA 10 Figure 5.13 related to poor hospital standards. Strict attention to ward cleanliness, gloving before touching patient wounds and hand - washing between all patient contacts are important preventive measures. An outbreak of  wound infections on the ward with bacteria having the same antibiotic sensitivity profile implies an exogenous source of  infection, which needs to be investigated by swabbing all sta ff and work surfaces. It may need temporary ward closure and a deep clean to eradicate the infection source. Now that patients are discharged more quickly after sur - gery and many procedures are performed as day cases, many SSIs are missed by the surgical team unless they undertake a prolonged and carefully audited follow-up with primary care doctors. Suppurative wound infections take 7–10 days to elop, and even cellulitis around wounds caused by inva - dev sive organisms (such as β -haemolytic Streptococcus ) takes 3–4 days to develop. Major surgical infections with systemic signs ( Figure 5.13 ), evidence of spreading infection, cellulitis or bacteraemia need treatment with appropriate antibiotics. The choice may need to be empirical initially but is best based on culture and sensitivities of  isolates harvested at surgery or from e of  wound fluids or wound swabs. Although the iden - cultur tification of  organisms in surgical infections is necessary for audit and wound surveillance purposes, it is usually 2–3 days before sensitivities are known ( Figures 5.14 and 5.15 ) . It is illogical to withhold antibiotics until results are available but, if  clinical response is poor by the time sensitivities are known, then antibiotics can be changed. Such changes are unusual if choice of antibiotics is sensible; change of  anti - the empirical biotics promotes resistance and risks complications, such as C. di ff . enteritis. If  an infected wound is under tension, or there is clear evi - dence of  suppuration, sutures or clips need to be removed, with curettage if  necessary , to allow pus to drain adequately . In severely contaminated wounds, such as an incision made for drainage of  an abscess, it is logical to lea ve the skin open. Delayed primary or secondary closure can be undertaken when the wound is clean and granulating ( Figures 5.16 and 5.17 ) . 250 240 Some heavily infected wounds may be left to heal by secondary 230 intention, with no attempt at closure, particularly where there 220 210 is a loss of  skin cover and healthy granulation tissue develops 200 190 BLOOD PRESSURE mmHg 180 170 160 150 140 130 120 110 100 90 80 70 60 Figure 5.14 

Classic swinging pyrexia related to a perianastomotic
wound abscess that settled spontaneously on antibiotic therapy.
Mixed streptococcal infection of a skin graft with very
poor ‘take’.

Figure 5.15 Figure 5.14 (a) (b) Figure 5.16 (a, b) Figure 5.17 that can always be revised with plastic surgery under clean surgical conditions at a later stage ( Summary box 5.13 ). Summary box 5.13 Surgical incisions through infected or contaminated tissues /uni25CF /uni25CF /uni25CF When taking pus from infected wounds, specimens should be sent fresh for microbiological culture. Swabs should be placed in transport medium, but the larger the volume of  pus sent, the more likely is the accurate identification of  the organ - ism involved. Providing the microbiologist with as much infor - mation as possible and discussing the results with them gives the best chance of  the most appropriate antibiotic treatment. If bacteraemia is suspected, but results are nega tive, then repeat specimens for blood culture and an immediate Gram stain. Topical antiseptics should only be used on heavily con - taminated wounds for a short period to clear infection as they inhibit epithelial ingrowth and so impair wound healing. 

After 5–6 days of antibiotics, the infection shown in
is under control, and the skin grafts are clearly viable.
Delayed primary closure of a fasciotomy wound
after 3–5 days.
Skin layers left open to granulate after laparotomy for
faecal peritonitis, ready for skin grafting.
When possible, tissue or pus for culture should be taken before
antibiotic cover is started
The choice of antibiotics is empirical until sensitivities are
available
Heavily contaminated wounds are best managed by delayed
primary or secondary closure

# Prophylactic antibiotics

Prophylactic antibiotics

Prophylactic antibiotics are used when there is a risk of  wound contamination with bacteria during surgery . The theoretical Council (USA) over 40 years ago, relates well to infection rates ( T able 5.2 ). The value of  antibiotic prophylaxis is low in non-prosthetic clean surgery , with most trials showing no clear benefit because infection rates without antibiotics are so low . The exception to this is where a prosthetic implant is used, as the results of  infection are so catastrophic that even a small risk of  infection is unacceptable. There is undisputed evidence that prophylactic antibiotics are e ff ective in reducing the risk of infection in clean-contaminated and contaminated operations. When wounds are heavily contaminated or when an incision is made into an abscess, a 5-day course of therapeutic antibiotics may be justified on the assumption that the wound is inevitably infected and so treatment is needed rather than prophylaxis. - If  antibiotics are given to prevent infection after surgery or instrumentation, they should be used before bacterial growth becomes established (i.e. within the decisive period). Ideally , maximal blood and tissue levels should be present at the time at which the first incision is made and before contamination occurs. Tissue levels of  the antibiotic should remain high throughout the operation and antibiotics with a short tissue half-life should be avoided. Intravenous administration at induction of  anaesthesia is therefore optimal, as unexpected delays in the timing of  surgery may occur before then and antibiotic tissue levels may fall o ff before the surgery starts. In long operations or when there is excessive blood loss, or instru - when unexpected contamination occurs, antibiotics may be repeated at 4-hourly intervals during the surgery because tis - - sue antibiotic levels often fall faster than serum levels. There is no evidence that further doses of  antibiotics after surgery are of any value in prophylaxis against infection and the practice can only encourage the development of antibiotic resistance. The choice of  an antibiotic depends on the expected spectrum of  organisms likely to be encountered, which will depend on the site and type of  surgery and whether the patient has any antibiotic allergies. Hospitals in the UK and across Europe now have standardised antibiotic prophylaxis policies that take account of the above factors and are only deviated from with microbiological advice. Patients with known valvular disease of  the heart (or with any implanted vascular or orthopaedic prosthesis) should have prophylactic antibiotics during dental, urological or open 

TABLE 5.2
Surgical site infection rates relating to wound
contamination with and without using antibiotic prophylaxis
Infection
Type of surgery
Infection
rate without
rate with
prophylaxis (%)
prophylaxis (%)
Clean (no viscus opened) 1–2
1–2
Clean-contaminated (viscus
3
6–9
opened, minimal spillage)
6
13–20
Contaminated (open viscus
with spillage or in
/f_l
ammatory
disease)
Dirty (pus or perforation, or
7
40
incision through an abscess)

prosthesis during the transient bacteraemia which can occur during such surgery ( Summary box 5.12 ). Summary box 5.12 Antibiotic prophylaxis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF 

Not required in clean surgery unless a prosthesis is implanted
Use antibiotics that are effective against expected pathogens
within local hospital guidelines
Plan for single-shot intravenous administration at induction of
anaesthesia
Repeat only during long operations or if there is excessive
blood loss
Patients with heart valve disease or a prosthesis should be
protected from bacteraemia caused by dental work, urethral
instrumentation or visceral surgery

Prophylactic antibiotics

Prophylactic antibiotics are used when there is a risk of  wound contamination with bacteria during surgery . The theoretical Council (USA) over 40 years ago, relates well to infection rates ( T able 5.2 ). The value of  antibiotic prophylaxis is low in non-prosthetic clean surgery , with most trials showing no clear benefit because infection rates without antibiotics are so low . The exception to this is where a prosthetic implant is used, as the results of  infection are so catastrophic that even a small risk of  infection is unacceptable. There is undisputed evidence that prophylactic antibiotics are e ff ective in reducing the risk of infection in clean-contaminated and contaminated operations. When wounds are heavily contaminated or when an incision is made into an abscess, a 5-day course of therapeutic antibiotics may be justified on the assumption that the wound is inevitably infected and so treatment is needed rather than prophylaxis. - If  antibiotics are given to prevent infection after surgery or instrumentation, they should be used before bacterial growth becomes established (i.e. within the decisive period). Ideally , maximal blood and tissue levels should be present at the time at which the first incision is made and before contamination occurs. Tissue levels of  the antibiotic should remain high throughout the operation and antibiotics with a short tissue half-life should be avoided. Intravenous administration at induction of  anaesthesia is therefore optimal, as unexpected delays in the timing of  surgery may occur before then and antibiotic tissue levels may fall o ff before the surgery starts. In long operations or when there is excessive blood loss, or instru - when unexpected contamination occurs, antibiotics may be repeated at 4-hourly intervals during the surgery because tis - - sue antibiotic levels often fall faster than serum levels. There is no evidence that further doses of  antibiotics after surgery are of any value in prophylaxis against infection and the practice can only encourage the development of antibiotic resistance. The choice of  an antibiotic depends on the expected spectrum of  organisms likely to be encountered, which will depend on the site and type of  surgery and whether the patient has any antibiotic allergies. Hospitals in the UK and across Europe now have standardised antibiotic prophylaxis policies that take account of the above factors and are only deviated from with microbiological advice. Patients with known valvular disease of  the heart (or with any implanted vascular or orthopaedic prosthesis) should have prophylactic antibiotics during dental, urological or open 

TABLE 5.2
Surgical site infection rates relating to wound
contamination with and without using antibiotic prophylaxis
Infection
Type of surgery
Infection
rate without
rate with
prophylaxis (%)
prophylaxis (%)
Clean (no viscus opened) 1–2
1–2
Clean-contaminated (viscus
3
6–9
opened, minimal spillage)
6
13–20
Contaminated (open viscus
with spillage or in
/f_l
ammatory
disease)
Dirty (pus or perforation, or
7
40
incision through an abscess)

prosthesis during the transient bacteraemia which can occur during such surgery ( Summary box 5.12 ). Summary box 5.12 Antibiotic prophylaxis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF 

Not required in clean surgery unless a prosthesis is implanted
Use antibiotics that are effective against expected pathogens
within local hospital guidelines
Plan for single-shot intravenous administration at induction of
anaesthesia
Repeat only during long operations or if there is excessive
blood loss
Patients with heart valve disease or a prosthesis should be
protected from bacteraemia caused by dental work, urethral
instrumentation or visceral surgery

Prophylactic antibiotics

Prophylactic antibiotics are used when there is a risk of  wound contamination with bacteria during surgery . The theoretical Council (USA) over 40 years ago, relates well to infection rates ( T able 5.2 ). The value of  antibiotic prophylaxis is low in non-prosthetic clean surgery , with most trials showing no clear benefit because infection rates without antibiotics are so low . The exception to this is where a prosthetic implant is used, as the results of  infection are so catastrophic that even a small risk of  infection is unacceptable. There is undisputed evidence that prophylactic antibiotics are e ff ective in reducing the risk of infection in clean-contaminated and contaminated operations. When wounds are heavily contaminated or when an incision is made into an abscess, a 5-day course of therapeutic antibiotics may be justified on the assumption that the wound is inevitably infected and so treatment is needed rather than prophylaxis. - If  antibiotics are given to prevent infection after surgery or instrumentation, they should be used before bacterial growth becomes established (i.e. within the decisive period). Ideally , maximal blood and tissue levels should be present at the time at which the first incision is made and before contamination occurs. Tissue levels of  the antibiotic should remain high throughout the operation and antibiotics with a short tissue half-life should be avoided. Intravenous administration at induction of  anaesthesia is therefore optimal, as unexpected delays in the timing of  surgery may occur before then and antibiotic tissue levels may fall o ff before the surgery starts. In long operations or when there is excessive blood loss, or instru - when unexpected contamination occurs, antibiotics may be repeated at 4-hourly intervals during the surgery because tis - - sue antibiotic levels often fall faster than serum levels. There is no evidence that further doses of  antibiotics after surgery are of any value in prophylaxis against infection and the practice can only encourage the development of antibiotic resistance. The choice of  an antibiotic depends on the expected spectrum of  organisms likely to be encountered, which will depend on the site and type of  surgery and whether the patient has any antibiotic allergies. Hospitals in the UK and across Europe now have standardised antibiotic prophylaxis policies that take account of the above factors and are only deviated from with microbiological advice. Patients with known valvular disease of  the heart (or with any implanted vascular or orthopaedic prosthesis) should have prophylactic antibiotics during dental, urological or open 

TABLE 5.2
Surgical site infection rates relating to wound
contamination with and without using antibiotic prophylaxis
Infection
Type of surgery
Infection
rate without
rate with
prophylaxis (%)
prophylaxis (%)
Clean (no viscus opened) 1–2
1–2
Clean-contaminated (viscus
3
6–9
opened, minimal spillage)
6
13–20
Contaminated (open viscus
with spillage or in
/f_l
ammatory
disease)
Dirty (pus or perforation, or
7
40
incision through an abscess)

prosthesis during the transient bacteraemia which can occur during such surgery ( Summary box 5.12 ). Summary box 5.12 Antibiotic prophylaxis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF 

Not required in clean surgery unless a prosthesis is implanted
Use antibiotics that are effective against expected pathogens
within local hospital guidelines
Plan for single-shot intravenous administration at induction of
anaesthesia
Repeat only during long operations or if there is excessive
blood loss
Patients with heart valve disease or a prosthesis should be
protected from bacteraemia caused by dental work, urethral
instrumentation or visceral surgery

# Reduced resistance to infection

Reduced resistance to infection

Reduced resistance to infection has several causes, particularly those that impair the inflammatory response. Host response is weakened by malnutrition associated with a low or high body mass index. Metabolic diseases such as diabetes mellitus, uraemia and jaundice, disseminated malignancy and acquired immunodeficiency syndrome (AIDS) are other contributors to infection and a poor healing response, as are iatrogenic causes including the immunosuppression caused by radiotherapy , chemotherapy and drugs such as steroids and methotrexate - ( Figures 5.4 and 5.5 ) . When enteral feeding is suspended during the perioperative period, and particularly with underlying disease such as can - cer, immunosuppression, shock or sepsis, bacteria (particularly aerobic Gram-negative bacilli) tend to colonise the normally sterile upper gastrointestinal tract. T hey may then translocate Figure 5.4 Figure 5.5 to the mesenteric nodes and cause the release of endotoxins (lipopolysaccharide in bacterial cell walls), which can be one cause of  a harmful systemic inflammatory response through the excessive release of  proinflammatory cytokines and acti vation of macrophages ( Figure 5.6 ). In the circumstances reduced host resistance to infection, microorganisms that are not normally pathogenic may start to behav e as pathogens. This is known as opportunistic infection. Opportunistic infec tion with fungi is an example, particularly when prolonged and changing antibiotic regimes have been used. 

Major wound infection and delayed healing presenting as
a faecal
/f_i
stula in a patient with Crohn’s disease on steroid treatment.
Delayed healing relating to infection in a patient on high-
dose steroids.

Reduced resistance to infection

Reduced resistance to infection has several causes, particularly those that impair the inflammatory response. Host response is weakened by malnutrition associated with a low or high body mass index. Metabolic diseases such as diabetes mellitus, uraemia and jaundice, disseminated malignancy and acquired immunodeficiency syndrome (AIDS) are other contributors to infection and a poor healing response, as are iatrogenic causes including the immunosuppression caused by radiotherapy , chemotherapy and drugs such as steroids and methotrexate - ( Figures 5.4 and 5.5 ) . When enteral feeding is suspended during the perioperative period, and particularly with underlying disease such as can - cer, immunosuppression, shock or sepsis, bacteria (particularly aerobic Gram-negative bacilli) tend to colonise the normally sterile upper gastrointestinal tract. T hey may then translocate Figure 5.4 Figure 5.5 to the mesenteric nodes and cause the release of endotoxins (lipopolysaccharide in bacterial cell walls), which can be one cause of  a harmful systemic inflammatory response through the excessive release of  proinflammatory cytokines and acti vation of macrophages ( Figure 5.6 ). In the circumstances reduced host resistance to infection, microorganisms that are not normally pathogenic may start to behav e as pathogens. This is known as opportunistic infection. Opportunistic infec tion with fungi is an example, particularly when prolonged and changing antibiotic regimes have been used. 

Major wound infection and delayed healing presenting as
a faecal
/f_i
stula in a patient with Crohn’s disease on steroid treatment.
Delayed healing relating to infection in a patient on high-
dose steroids.

Reduced resistance to infection

Reduced resistance to infection has several causes, particularly those that impair the inflammatory response. Host response is weakened by malnutrition associated with a low or high body mass index. Metabolic diseases such as diabetes mellitus, uraemia and jaundice, disseminated malignancy and acquired immunodeficiency syndrome (AIDS) are other contributors to infection and a poor healing response, as are iatrogenic causes including the immunosuppression caused by radiotherapy , chemotherapy and drugs such as steroids and methotrexate - ( Figures 5.4 and 5.5 ) . When enteral feeding is suspended during the perioperative period, and particularly with underlying disease such as can - cer, immunosuppression, shock or sepsis, bacteria (particularly aerobic Gram-negative bacilli) tend to colonise the normally sterile upper gastrointestinal tract. T hey may then translocate Figure 5.4 Figure 5.5 to the mesenteric nodes and cause the release of endotoxins (lipopolysaccharide in bacterial cell walls), which can be one cause of  a harmful systemic inflammatory response through the excessive release of  proinflammatory cytokines and acti vation of macrophages ( Figure 5.6 ). In the circumstances reduced host resistance to infection, microorganisms that are not normally pathogenic may start to behav e as pathogens. This is known as opportunistic infection. Opportunistic infec tion with fungi is an example, particularly when prolonged and changing antibiotic regimes have been used. 

Major wound infection and delayed healing presenting as
a faecal
/f_i
stula in a patient with Crohn’s disease on steroid treatment.
Delayed healing relating to infection in a patient on high-
dose steroids.

# Sources of infection

Sources of infection

- The infection of  a wound can be defined as the invasion of - organisms into tissues following a breakdown of  local and systemic host defences, leading to cellulitis, lymphangitis, abscess formation or bacteraemia. The infection of  most surgi - cal wounds is referred to as superficial surgical site infection (SSSI). The other categories include deep SSI (infection in the deeper musculofascial layers) and organ space infection (such abscess after a perforated appendicitis). Pathogens resist host defences by releasing toxins, which favour their spread, and this is enhanced in anaerobic or frankly necrotic wound tissue. Clostridium perfringens , which is responsible for gas gangrene, releases proteases such as hyalu ronidase, lecithinase and haemolysin, which allow it to spread through the tissues. Resistance to antibiotics can be acquired by previously sensitive bacteria by transfer through plasmids. 14 The human body harbours approximately 10 organisms. They can be released into tissues before, during or after sur gery , contamination being most severe when a hollow viscus perforates (e.g. faecal peritonitis following a diverticular per foration). Any infection that follows surgery may be termed endogenous or exogenous, depending on the source of the bacterial contamination. Endogenous organisms are present on or in the patient at the time of  surger y , whereas exogenous organisms come from outside the patient. In modern hospital practice, endogenous organisms colonising the patient are by far the most common source of  infection ( Summary box 5.3 Summary box 5.3 Classification of sources of infection /uni25CF /uni25CF Microorganisms are normally prevented from causing infection in tissues by intact epithelial surfaces, most notably the skin. These surfaces are broken down by trauma or surgery . In addition to these mechanical barriers, there are other pro tective mechanisms, which can be divided into: /uni25CF chemical : low gastric pH; /uni25CF humoral : antibodies, complement and opsonins; /uni25CF cellular : phagocytic cells, macrophages, polymorphonu clear cells and killer lymphocytes. All of  these natural mechanisms may be compromised by surgical intervention and treatment. The chance of  developing an SSI after surgery is also determined by the pathogenicity of  the organisms pr esent and by the size of the bacterial inoculum. The more virulent the organism or the larger the extent of  bacterial contamination, the more likely is wound infection to occur. Host factors are also important, so a less virulent organism or a lower level of wound contamination may still result in a wound infection if the host response is impaired ( Summary box 5.4 ). Devital ised tissue, excessive dead space or haematoma, which are all the results of  poor surgical technique, increase the chances of infection. The same applies to foreign materials of  any kind, including sutures and drains . These principles are important to an understanding of how best to prevent infection in surgical practice ( Summary box 5.5 ). Factors that determine whether a wound will become infected /uni25CF - /uni25CF /uni25CF /uni25CF /uni25CF - - Summary box 5.5 Risk factors for increased risk of wound infection /uni25CF /uni25CF /uni25CF ). /uni25CF /uni25CF /uni25CF /uni25CF 

Endogenous
: present in or on the host, e.g. SSSI following
contamination of the wound from a perforated appendix
Exogenous
: acquired from a source outside the body, such as
the operating theatre (inadequate air
/f_i
ltration, poor antisepsis)
or the ward (e.g. poor handwashing compliance). The cause of
hospital-acquired infection (HAI)
Host response
Virulence and inoculum of infective agent
Vascularity and health of tissue being invaded (including local
ischaemia as well as systemic shock)
Presence of dead or foreign tissue
Presence of antibiotics during the ‘decisive period’
Malnutrition (obesity, weight loss)
Metabolic disease (diabetes, uraemia, jaundice)
Immunosuppression (cancer, acquired immunode
/f_i
ciency
syndrome [AIDS], steroids, chemotherapy and radiotherapy)
Colonisation and translocation in the gastrointestinal tract
Poor perfusion (systemic shock or local ischaemia)
Foreign body material
Poor surgical technique (devitalised tissue, dead space,
haematoma)

Sources of infection

- The infection of  a wound can be defined as the invasion of - organisms into tissues following a breakdown of  local and systemic host defences, leading to cellulitis, lymphangitis, abscess formation or bacteraemia. The infection of  most surgi - cal wounds is referred to as superficial surgical site infection (SSSI). The other categories include deep SSI (infection in the deeper musculofascial layers) and organ space infection (such abscess after a perforated appendicitis). Pathogens resist host defences by releasing toxins, which favour their spread, and this is enhanced in anaerobic or frankly necrotic wound tissue. Clostridium perfringens , which is responsible for gas gangrene, releases proteases such as hyalu ronidase, lecithinase and haemolysin, which allow it to spread through the tissues. Resistance to antibiotics can be acquired by previously sensitive bacteria by transfer through plasmids. 14 The human body harbours approximately 10 organisms. They can be released into tissues before, during or after sur gery , contamination being most severe when a hollow viscus perforates (e.g. faecal peritonitis following a diverticular per foration). Any infection that follows surgery may be termed endogenous or exogenous, depending on the source of the bacterial contamination. Endogenous organisms are present on or in the patient at the time of  surger y , whereas exogenous organisms come from outside the patient. In modern hospital practice, endogenous organisms colonising the patient are by far the most common source of  infection ( Summary box 5.3 Summary box 5.3 Classification of sources of infection /uni25CF /uni25CF Microorganisms are normally prevented from causing infection in tissues by intact epithelial surfaces, most notably the skin. These surfaces are broken down by trauma or surgery . In addition to these mechanical barriers, there are other pro tective mechanisms, which can be divided into: /uni25CF chemical : low gastric pH; /uni25CF humoral : antibodies, complement and opsonins; /uni25CF cellular : phagocytic cells, macrophages, polymorphonu clear cells and killer lymphocytes. All of  these natural mechanisms may be compromised by surgical intervention and treatment. The chance of  developing an SSI after surgery is also determined by the pathogenicity of  the organisms pr esent and by the size of the bacterial inoculum. The more virulent the organism or the larger the extent of  bacterial contamination, the more likely is wound infection to occur. Host factors are also important, so a less virulent organism or a lower level of wound contamination may still result in a wound infection if the host response is impaired ( Summary box 5.4 ). Devital ised tissue, excessive dead space or haematoma, which are all the results of  poor surgical technique, increase the chances of infection. The same applies to foreign materials of  any kind, including sutures and drains . These principles are important to an understanding of how best to prevent infection in surgical practice ( Summary box 5.5 ). Factors that determine whether a wound will become infected /uni25CF - /uni25CF /uni25CF /uni25CF /uni25CF - - Summary box 5.5 Risk factors for increased risk of wound infection /uni25CF /uni25CF /uni25CF ). /uni25CF /uni25CF /uni25CF /uni25CF 

Endogenous
: present in or on the host, e.g. SSSI following
contamination of the wound from a perforated appendix
Exogenous
: acquired from a source outside the body, such as
the operating theatre (inadequate air
/f_i
ltration, poor antisepsis)
or the ward (e.g. poor handwashing compliance). The cause of
hospital-acquired infection (HAI)
Host response
Virulence and inoculum of infective agent
Vascularity and health of tissue being invaded (including local
ischaemia as well as systemic shock)
Presence of dead or foreign tissue
Presence of antibiotics during the ‘decisive period’
Malnutrition (obesity, weight loss)
Metabolic disease (diabetes, uraemia, jaundice)
Immunosuppression (cancer, acquired immunode
/f_i
ciency
syndrome [AIDS], steroids, chemotherapy and radiotherapy)
Colonisation and translocation in the gastrointestinal tract
Poor perfusion (systemic shock or local ischaemia)
Foreign body material
Poor surgical technique (devitalised tissue, dead space,
haematoma)

Sources of infection

- The infection of  a wound can be defined as the invasion of - organisms into tissues following a breakdown of  local and systemic host defences, leading to cellulitis, lymphangitis, abscess formation or bacteraemia. The infection of  most surgi - cal wounds is referred to as superficial surgical site infection (SSSI). The other categories include deep SSI (infection in the deeper musculofascial layers) and organ space infection (such abscess after a perforated appendicitis). Pathogens resist host defences by releasing toxins, which favour their spread, and this is enhanced in anaerobic or frankly necrotic wound tissue. Clostridium perfringens , which is responsible for gas gangrene, releases proteases such as hyalu ronidase, lecithinase and haemolysin, which allow it to spread through the tissues. Resistance to antibiotics can be acquired by previously sensitive bacteria by transfer through plasmids. 14 The human body harbours approximately 10 organisms. They can be released into tissues before, during or after sur gery , contamination being most severe when a hollow viscus perforates (e.g. faecal peritonitis following a diverticular per foration). Any infection that follows surgery may be termed endogenous or exogenous, depending on the source of the bacterial contamination. Endogenous organisms are present on or in the patient at the time of  surger y , whereas exogenous organisms come from outside the patient. In modern hospital practice, endogenous organisms colonising the patient are by far the most common source of  infection ( Summary box 5.3 Summary box 5.3 Classification of sources of infection /uni25CF /uni25CF Microorganisms are normally prevented from causing infection in tissues by intact epithelial surfaces, most notably the skin. These surfaces are broken down by trauma or surgery . In addition to these mechanical barriers, there are other pro tective mechanisms, which can be divided into: /uni25CF chemical : low gastric pH; /uni25CF humoral : antibodies, complement and opsonins; /uni25CF cellular : phagocytic cells, macrophages, polymorphonu clear cells and killer lymphocytes. All of  these natural mechanisms may be compromised by surgical intervention and treatment. The chance of  developing an SSI after surgery is also determined by the pathogenicity of  the organisms pr esent and by the size of the bacterial inoculum. The more virulent the organism or the larger the extent of  bacterial contamination, the more likely is wound infection to occur. Host factors are also important, so a less virulent organism or a lower level of wound contamination may still result in a wound infection if the host response is impaired ( Summary box 5.4 ). Devital ised tissue, excessive dead space or haematoma, which are all the results of  poor surgical technique, increase the chances of infection. The same applies to foreign materials of  any kind, including sutures and drains . These principles are important to an understanding of how best to prevent infection in surgical practice ( Summary box 5.5 ). Factors that determine whether a wound will become infected /uni25CF - /uni25CF /uni25CF /uni25CF /uni25CF - - Summary box 5.5 Risk factors for increased risk of wound infection /uni25CF /uni25CF /uni25CF ). /uni25CF /uni25CF /uni25CF /uni25CF 

Endogenous
: present in or on the host, e.g. SSSI following
contamination of the wound from a perforated appendix
Exogenous
: acquired from a source outside the body, such as
the operating theatre (inadequate air
/f_i
ltration, poor antisepsis)
or the ward (e.g. poor handwashing compliance). The cause of
hospital-acquired infection (HAI)
Host response
Virulence and inoculum of infective agent
Vascularity and health of tissue being invaded (including local
ischaemia as well as systemic shock)
Presence of dead or foreign tissue
Presence of antibiotics during the ‘decisive period’
Malnutrition (obesity, weight loss)
Metabolic disease (diabetes, uraemia, jaundice)
Immunosuppression (cancer, acquired immunode
/f_i
ciency
syndrome [AIDS], steroids, chemotherapy and radiotherapy)
Colonisation and translocation in the gastrointestinal tract
Poor perfusion (systemic shock or local ischaemia)
Foreign body material
Poor surgical technique (devitalised tissue, dead space,
haematoma)

# Systemic infection Bacteraemia

Systemic infection Bacteraemia

Bacteraemia is unusual following superficial SSIs, which tend to drain through the wound, but common after deep space SSIs, such as following an intestinal anastomotic breakdown. It is usually transient and can follow procedures undertaken through infected tissues (particularly instrumentation in infected bile or urine). It may also occur through bacterial infection of  indwelling intravenous cannulae, which should be replaced regularly to avoid colonisation. Bacteraemia is important when a prosthesis has been implanted, as infection of  the prosthesis can occur through haematogenous spread. Aerobic Gram-negative bacilli are often responsible, but Staphylococcus aureus and fungi may be involved ( Summary box 5.10 ). Summary box 5.10 Bacteraemia /uni25CF /uni25CF /uni25CF 

Common after anastomotic breakdown
Dangerous if the patient has a prosthesis, which can become
infected
May be associated with systemic organ failure

Systemic infection Bacteraemia

Bacteraemia is unusual following superficial SSIs, which tend to drain through the wound, but common after deep space SSIs, such as following an intestinal anastomotic breakdown. It is usually transient and can follow procedures undertaken through infected tissues (particularly instrumentation in infected bile or urine). It may also occur through bacterial infection of  indwelling intravenous cannulae, which should be replaced regularly to avoid colonisation. Bacteraemia is important when a prosthesis has been implanted, as infection of  the prosthesis can occur through haematogenous spread. Aerobic Gram-negative bacilli are often responsible, but Staphylococcus aureus and fungi may be involved ( Summary box 5.10 ). Summary box 5.10 Bacteraemia /uni25CF /uni25CF /uni25CF 

Common after anastomotic breakdown
Dangerous if the patient has a prosthesis, which can become
infected
May be associated with systemic organ failure

Systemic infection Bacteraemia

Bacteraemia is unusual following superficial SSIs, which tend to drain through the wound, but common after deep space SSIs, such as following an intestinal anastomotic breakdown. It is usually transient and can follow procedures undertaken through infected tissues (particularly instrumentation in infected bile or urine). It may also occur through bacterial infection of  indwelling intravenous cannulae, which should be replaced regularly to avoid colonisation. Bacteraemia is important when a prosthesis has been implanted, as infection of  the prosthesis can occur through haematogenous spread. Aerobic Gram-negative bacilli are often responsible, but Staphylococcus aureus and fungi may be involved ( Summary box 5.10 ). Summary box 5.10 Bacteraemia /uni25CF /uni25CF /uni25CF 

Common after anastomotic breakdown
Dangerous if the patient has a prosthesis, which can become
infected
May be associated with systemic organ failure

# Systemic inflammatory response syndrome

Systemic inflammatory response syndrome

Systemic inflammatory response syndrome (SIRS) is a systemic manifestation of  sepsis ( Table 5.1 ), although the syndrome may also be caused by multiple trauma, burns or pancreatitis without infection. Serious infection, such as secondary peritonitis, may lead to SIRS through the release of  lipopolysaccharide endo - toxin from the walls of  dying Gram-negative bacilli (mainly Escherichia coli ) or other bacteria or fungi. This and other toxins stimulate the release of cytokines from macrophages ( Figure 5.6 ). SIRS should not be confused with bacteraemia, although the two may coexist. /uni25CF /uni25CF β /uni25CF Septic manifestations and multiple organ dysfunction syn drome (MODS) in SIRS are mediated by the release of  pro inflammatory cytokines such as interleukin-1 (IL-1) and tumour necrosis factor alpha (TNF α ). These cytokines normally stim ulate neutrophil adhesion to endothelial surfaces adjacent to the source of  infection and cause them to migrate through the blood vessel wall by chemotaxis , where they can a ttack the bacterial invasion. A respiratory burst occurs within such acti vated neutrophils, releasing lysosomal enzymes, oxidants and free radicals, which are involved in killing the invading bacte ria but which may also damage adjacent cells. Coagulation, complement and fibrinolytic pathways are also stimulated as part of the normal inflammatory response. This response is usually beneficial to the host and is an important aspect of normal tissue repair and wound healing. On occasions, this response may become harmful to the host if  it occurs in excess, when it is known as the systemic inflammatory response syn drome or SIRS. There are high circulating levels of  cytokines and activated neutrophils that stimulate fever, tachycardia and tachypnoea. The activa ted neutrophils adhere to vascular endothelium in key organs remote from the source of  infec tion and damage it, leading to increased vascular permeability , which in turn leads to cellular damage within the organs, which become dysfunctional and give rise to the clinical picture of multiple organ dysfunction syndrome or MODS. In its most se vere form, MODS may progress into multiple system organ failure (MSOF). Respiratory , cardiac, intestinal, renal and liver failure ensue in combination with circulatory failure and shock. In this state, the body’s resistance to infection is reduced and a vicious cycle develops where the more organs that fail, the more likely it becomes that death will follow despite all that a modern ICU can do for organ support ( Summary box 5.11 Summary box 5.11 Definitions of infected states /uni25CF /uni25CF /uni25CF /uni25CF Moritz Kaposi, 1837–1902, Professor of  Dermatology , Vienna, Austria, described pigmented sarcoma of  the skin in 1872. Sepsis Six The European Society of  Intensive Care Medicine (ESICM) alongside the Society of  Critical Care Medicine (SCCM) spearheaded the Surviving Sepsis Campaign (SSC) in 2002 with several aims, including the development of  guidelines for the diagnosis, treatment and post-ICU care of sepsis and a reduction in mortality from sepsis. The Surviving Sepsis Campaign continually develops and updates resources and implementation tools to further its mission of  reducing sepsis and septic shock. The sepsis bundle , also known as the resuscitation bun - dle, is a combination of  evidence-based objectives that must be completed within 6 hours for patients presenting with severe sepsis, septic shock and/or lactate >4 /uni00A0 mmol/L. - The Sepsis Six is the name given to a bundle of  medical - therapies designed to reduce mortality in patients with sepsis. Drawn from international guidelines that emerged from the - Surviving Sepsis Campaign, the Sepsis Six was developed by the UK’s Sepsis Trust. The components of  the Sepsis Six are: /uni25CF give three to patients: (1) intravenous fluid challenge, (2) intravenous antibiotics, (3) oxygen and monitor urine - output; /uni25CF take three from patients: (4) blood cultures, (5) full - blood count, (6) lactate. 

syndrome (SIRS) and sepsis
SIRS
is
Presence of two out of three of the following:
Hyperthermia (>38°C) or hypothermia (<36°C)
Tachycardia (>90/min, no
-blockers) or tachypnoea (>20/min)
9
9
White cell count >12
/uni00A0×/uni00A0
10
/litre or <4
×
10
/litre
Sepsis
is SIRS with a documented source of infection
Severe sepsis or sepsis syndrome
is sepsis with evidence
of failure of one or more organs: respiratory (acute respiratory
distress syndrome), cardiovascular (septic shock follows
compromise of cardiac function and fall in peripheral vascular
resistance), renal (usually acute tubular necrosis), hepatic, blood
coagulation systems or central nervous system
SSI is an infected wound or deep organ space
SIRS is the body’s systemic response to severe infection
MODS is the effect that SIRS produces systemically
MSOF is the end stage of uncontrolled MODS

Systemic inflammatory response syndrome

Systemic inflammatory response syndrome (SIRS) is a systemic manifestation of  sepsis ( Table 5.1 ), although the syndrome may also be caused by multiple trauma, burns or pancreatitis without infection. Serious infection, such as secondary peritonitis, may lead to SIRS through the release of  lipopolysaccharide endo - toxin from the walls of  dying Gram-negative bacilli (mainly Escherichia coli ) or other bacteria or fungi. This and other toxins stimulate the release of cytokines from macrophages ( Figure 5.6 ). SIRS should not be confused with bacteraemia, although the two may coexist. /uni25CF /uni25CF β /uni25CF Septic manifestations and multiple organ dysfunction syn drome (MODS) in SIRS are mediated by the release of  pro inflammatory cytokines such as interleukin-1 (IL-1) and tumour necrosis factor alpha (TNF α ). These cytokines normally stim ulate neutrophil adhesion to endothelial surfaces adjacent to the source of  infection and cause them to migrate through the blood vessel wall by chemotaxis , where they can a ttack the bacterial invasion. A respiratory burst occurs within such acti vated neutrophils, releasing lysosomal enzymes, oxidants and free radicals, which are involved in killing the invading bacte ria but which may also damage adjacent cells. Coagulation, complement and fibrinolytic pathways are also stimulated as part of the normal inflammatory response. This response is usually beneficial to the host and is an important aspect of normal tissue repair and wound healing. On occasions, this response may become harmful to the host if  it occurs in excess, when it is known as the systemic inflammatory response syn drome or SIRS. There are high circulating levels of  cytokines and activated neutrophils that stimulate fever, tachycardia and tachypnoea. The activa ted neutrophils adhere to vascular endothelium in key organs remote from the source of  infec tion and damage it, leading to increased vascular permeability , which in turn leads to cellular damage within the organs, which become dysfunctional and give rise to the clinical picture of multiple organ dysfunction syndrome or MODS. In its most se vere form, MODS may progress into multiple system organ failure (MSOF). Respiratory , cardiac, intestinal, renal and liver failure ensue in combination with circulatory failure and shock. In this state, the body’s resistance to infection is reduced and a vicious cycle develops where the more organs that fail, the more likely it becomes that death will follow despite all that a modern ICU can do for organ support ( Summary box 5.11 Summary box 5.11 Definitions of infected states /uni25CF /uni25CF /uni25CF /uni25CF Moritz Kaposi, 1837–1902, Professor of  Dermatology , Vienna, Austria, described pigmented sarcoma of  the skin in 1872. Sepsis Six The European Society of  Intensive Care Medicine (ESICM) alongside the Society of  Critical Care Medicine (SCCM) spearheaded the Surviving Sepsis Campaign (SSC) in 2002 with several aims, including the development of  guidelines for the diagnosis, treatment and post-ICU care of sepsis and a reduction in mortality from sepsis. The Surviving Sepsis Campaign continually develops and updates resources and implementation tools to further its mission of  reducing sepsis and septic shock. The sepsis bundle , also known as the resuscitation bun - dle, is a combination of  evidence-based objectives that must be completed within 6 hours for patients presenting with severe sepsis, septic shock and/or lactate >4 /uni00A0 mmol/L. - The Sepsis Six is the name given to a bundle of  medical - therapies designed to reduce mortality in patients with sepsis. Drawn from international guidelines that emerged from the - Surviving Sepsis Campaign, the Sepsis Six was developed by the UK’s Sepsis Trust. The components of  the Sepsis Six are: /uni25CF give three to patients: (1) intravenous fluid challenge, (2) intravenous antibiotics, (3) oxygen and monitor urine - output; /uni25CF take three from patients: (4) blood cultures, (5) full - blood count, (6) lactate. 

syndrome (SIRS) and sepsis
SIRS
is
Presence of two out of three of the following:
Hyperthermia (>38°C) or hypothermia (<36°C)
Tachycardia (>90/min, no
-blockers) or tachypnoea (>20/min)
9
9
White cell count >12
/uni00A0×/uni00A0
10
/litre or <4
×
10
/litre
Sepsis
is SIRS with a documented source of infection
Severe sepsis or sepsis syndrome
is sepsis with evidence
of failure of one or more organs: respiratory (acute respiratory
distress syndrome), cardiovascular (septic shock follows
compromise of cardiac function and fall in peripheral vascular
resistance), renal (usually acute tubular necrosis), hepatic, blood
coagulation systems or central nervous system
SSI is an infected wound or deep organ space
SIRS is the body’s systemic response to severe infection
MODS is the effect that SIRS produces systemically
MSOF is the end stage of uncontrolled MODS

Systemic inflammatory response syndrome

Systemic inflammatory response syndrome (SIRS) is a systemic manifestation of  sepsis ( Table 5.1 ), although the syndrome may also be caused by multiple trauma, burns or pancreatitis without infection. Serious infection, such as secondary peritonitis, may lead to SIRS through the release of  lipopolysaccharide endo - toxin from the walls of  dying Gram-negative bacilli (mainly Escherichia coli ) or other bacteria or fungi. This and other toxins stimulate the release of cytokines from macrophages ( Figure 5.6 ). SIRS should not be confused with bacteraemia, although the two may coexist. /uni25CF /uni25CF β /uni25CF Septic manifestations and multiple organ dysfunction syn drome (MODS) in SIRS are mediated by the release of  pro inflammatory cytokines such as interleukin-1 (IL-1) and tumour necrosis factor alpha (TNF α ). These cytokines normally stim ulate neutrophil adhesion to endothelial surfaces adjacent to the source of  infection and cause them to migrate through the blood vessel wall by chemotaxis , where they can a ttack the bacterial invasion. A respiratory burst occurs within such acti vated neutrophils, releasing lysosomal enzymes, oxidants and free radicals, which are involved in killing the invading bacte ria but which may also damage adjacent cells. Coagulation, complement and fibrinolytic pathways are also stimulated as part of the normal inflammatory response. This response is usually beneficial to the host and is an important aspect of normal tissue repair and wound healing. On occasions, this response may become harmful to the host if  it occurs in excess, when it is known as the systemic inflammatory response syn drome or SIRS. There are high circulating levels of  cytokines and activated neutrophils that stimulate fever, tachycardia and tachypnoea. The activa ted neutrophils adhere to vascular endothelium in key organs remote from the source of  infec tion and damage it, leading to increased vascular permeability , which in turn leads to cellular damage within the organs, which become dysfunctional and give rise to the clinical picture of multiple organ dysfunction syndrome or MODS. In its most se vere form, MODS may progress into multiple system organ failure (MSOF). Respiratory , cardiac, intestinal, renal and liver failure ensue in combination with circulatory failure and shock. In this state, the body’s resistance to infection is reduced and a vicious cycle develops where the more organs that fail, the more likely it becomes that death will follow despite all that a modern ICU can do for organ support ( Summary box 5.11 Summary box 5.11 Definitions of infected states /uni25CF /uni25CF /uni25CF /uni25CF Moritz Kaposi, 1837–1902, Professor of  Dermatology , Vienna, Austria, described pigmented sarcoma of  the skin in 1872. Sepsis Six The European Society of  Intensive Care Medicine (ESICM) alongside the Society of  Critical Care Medicine (SCCM) spearheaded the Surviving Sepsis Campaign (SSC) in 2002 with several aims, including the development of  guidelines for the diagnosis, treatment and post-ICU care of sepsis and a reduction in mortality from sepsis. The Surviving Sepsis Campaign continually develops and updates resources and implementation tools to further its mission of  reducing sepsis and septic shock. The sepsis bundle , also known as the resuscitation bun - dle, is a combination of  evidence-based objectives that must be completed within 6 hours for patients presenting with severe sepsis, septic shock and/or lactate >4 /uni00A0 mmol/L. - The Sepsis Six is the name given to a bundle of  medical - therapies designed to reduce mortality in patients with sepsis. Drawn from international guidelines that emerged from the - Surviving Sepsis Campaign, the Sepsis Six was developed by the UK’s Sepsis Trust. The components of  the Sepsis Six are: /uni25CF give three to patients: (1) intravenous fluid challenge, (2) intravenous antibiotics, (3) oxygen and monitor urine - output; /uni25CF take three from patients: (4) blood cultures, (5) full - blood count, (6) lactate. 

syndrome (SIRS) and sepsis
SIRS
is
Presence of two out of three of the following:
Hyperthermia (>38°C) or hypothermia (<36°C)
Tachycardia (>90/min, no
-blockers) or tachypnoea (>20/min)
9
9
White cell count >12
/uni00A0×/uni00A0
10
/litre or <4
×
10
/litre
Sepsis
is SIRS with a documented source of infection
Severe sepsis or sepsis syndrome
is sepsis with evidence
of failure of one or more organs: respiratory (acute respiratory
distress syndrome), cardiovascular (septic shock follows
compromise of cardiac function and fall in peripheral vascular
resistance), renal (usually acute tubular necrosis), hepatic, blood
coagulation systems or central nervous system
SSI is an infected wound or deep organ space
SIRS is the body’s systemic response to severe infection
MODS is the effect that SIRS produces systemically
MSOF is the end stage of uncontrolled MODS

# The decisive period

The decisive period

There is up to a 4-hour interval before bacterial growth becomes established enough to cause an infection after a breach in the tissues, whether caused by trauma or by surgery . This interval is called the ‘decisive period’ and strategies aimed at preventing infection from taking a hold become ine ff ective after this time period. It is therefore logical that prophylactic antibiotics should be given to cover this period and that they could be - decisive in preventing an infection from developing before bacterial growth takes a hold. The tissue levels of  antibiotics during the period when bacterial contamination is likely to occur should be above the minimum inhibitory concentration (MIC90) for the expected pathogens. - The decisive period

There is up to a 4-hour interval before bacterial growth becomes established enough to cause an infection after a breach in the tissues, whether caused by trauma or by surgery . This interval is called the ‘decisive period’ and strategies aimed at preventing infection from taking a hold become ine ff ective after this time period. It is therefore logical that prophylactic antibiotics should be given to cover this period and that they could be - decisive in preventing an infection from developing before bacterial growth takes a hold. The tissue levels of  antibiotics during the period when bacterial contamination is likely to occur should be above the minimum inhibitory concentration (MIC90) for the expected pathogens. - The decisive period

There is up to a 4-hour interval before bacterial growth becomes established enough to cause an infection after a breach in the tissues, whether caused by trauma or by surgery . This interval is called the ‘decisive period’ and strategies aimed at preventing infection from taking a hold become ine ff ective after this time period. It is therefore logical that prophylactic antibiotics should be given to cover this period and that they could be - decisive in preventing an infection from developing before bacterial growth takes a hold. The tissue levels of  antibiotics during the period when bacterial contamination is likely to occur should be above the minimum inhibitory concentration (MIC90) for the expected pathogens. -

# Viral infections relevant to surgery

Viral infections relevant to surgery

Hepatitis Both hepatitis B and hepatitis C carry risks in surgery as they are blood-borne pathogens that can be transmitted both from - the patient to the surgeon and vice versa . The usual mode of transmission is blood-to-blood contact through a needle-stick injury or a cut. Many cases of  hepatitis B are asymptomatic and a surgeon may carry the virus without being aware of  it. As - there is an e ff ective vaccine against hepatitis B, surgeons should know their immune status to hepatitis B and be vaccinated against it. Hepatitis C infection often becomes chronic with the risk of  significant liver damage but is potentially curable with interferon-alpha and ribavirin treatment, so surgeons who are exposed to an infection risk should seek medical advice and antibody measurement. Human immunodeficiency virus The type I human immunodeficiency virus (HIV) is one of  the viruses of  surgical importance because it can be transmitted ). by body fluids, particularly blood. It is a retrovirus that has become increasingly prevalent through sexual transmission (both homo- and heterosexual), intravenous drug addiction and in infected blood products used to treat patients with haemophilia in particular. The risk in surgery is mostly through needle-stick injury during operations. The risk of  opportunistic infections (such as Pneumocystis carinii pneumonia, tuberculosis and cytomegalovirus) and neo - plasms (such as Kaposi’s sarcoma and lymphoma) is thereby increased. In the early weeks after HIV infection, there may be a flu like illness and, during the phase of  seroconversion, patients present the greatest risk of  HIV transmission. It is during these early phases that drug treatment, highly active antiretro therapy (HAART), is most e ff ective through the ability of  these drugs to inhibit reverse transcriptase and protease synthesis, which are the principal mechanisms through which HIV can progress. These drugs suppress the virus but do not clear it completely from the body and treated patients can still transmit the virus to others. Within 2 years, untreated HIV can progress to acquired immunodeficiency syndrome (AIDS) in 25–35% of  patients. Universal precautions Patients may present to surgeons for operative treatment if  they have a surgical disease and they are known to be infected or ‘at risk’, or because they need surgical intervention related to their illness for vascular access or a biopsy when they are known to have hepatitis, HIV infection or AIDS. Particular care should be taken when there is a risk of  splashing/aerosol formation, particularly with power tools. Universal precautions have been drawn up by CDC in the USA and largely adopted by the NHS in the UK. In summary , these are: /uni25CF use of  a full face mask ideally , or protective spectacles; /uni25CF use of  fully waterproof, disposable gowns and drapes, par ticularly during seroconversion; /uni25CF boots to be worn, not clogs, to avoid injury from dropped sharps; /uni25CF double gloving needed (a larger size on the inside is more comfortable); /uni25CF allow only essential personnel in theatre; /uni25CF avoid unnecessary movement in theatre; /uni25CF respect is required for sharps, with passage in a kidney dish; /uni25CF slow meticulous operative technique is needed with mini mised bleeding. After contamination Needle-stick injuries are commonest on the non-dominant index finger during operative surgery . Hollow needle injury carries the greatest risk of  viral transmission. The injured part should be washed under running water and the incident reported. Local policies dictate whether postexposure anti *Data from: COVID-19 dashboard by the Center for Systems Science and Engineering (CSSE) at Johns Hopkins University (accessed 16 August 2021). Figure 5.12 (a) (b) retroviral treatment should be given. Occupational health - advice is required after high-risk exposure, together with the need for hepatitis/HIV testing and the option for continuation in a non-operative specialty . viral COVID-19 pandemic The global pandemic of  coronavirus disease 2019 (COVID - 19) was announced by the World Health Organization on 11 March 2020. As of  16 August 2021, more than 207 million cases and more than 4.36 million deaths had been reported in 210 countries.* The rapid spread of  the outbreak has had short-term implications f or global healthcare systems, including the field of  surgery . Many hospitals were forced to stop or postpone elective surgical interventions during the first wave in early to mid-2020. However, emergency surgery and time-sensitive surgery , i.e. cancer surgery , continued with relevant precautions, including the use of  personal protective equipment. COVID-19 is a contagious respiratory and vascular dis - ease. The aetiology is severe acute respiratory syndrome coro - navirus 2 (SARS-CoV-2) ( Figure 5.12a ) , which is a specific type of  coronavirus. Common symptoms include fever, cough, fatigue, shortness of  breath or breathing di ffi culties as well as loss of  smell and taste . The incubation period may range from 1 to 14 days. While most people have mild symptoms, some - people develop acute respiratory distress syndrome (ARDS), possibly precipitated by a cytokine storm; multiorgan failure; septic shock; and hypercoagulable states. Longer term damage to organs (in particular, the lungs and heart) has been observed. Complications in postoperative surgical patients infected with COVID-19 in either an elective or emergency setting may include pneumonia ( Figure 5.12b ) , ARDS, multiorgan failure, se ptic shock and death. Measures to control COVID-19 - related morbidity and mortality have thus been implemented - by many countries, including a mandatory preopera tive cocooning of  elective surgical patients 10–14 days prior to sur - gery and preopera tive COVID-19 swab testing 2–3 days prior to elective surgery . Like many other viral infections, there is no definite pharmacological cure for this infection, although there has been some evidence for supportive care, e .g. with hydroxy - chloroquine and dexamethasone. Multiple vaccines were made available at the end of 2020 and, currently , the majority - of  countries have most of  their population vaccinated. 

Severe acute
respiratory syndrome coronavirus 2
(SARS-CoV-2).
Chest radiograph
showing coronavirus disease 2019
(COVID-19) pneumonia changes.

Viral infections relevant to surgery

Hepatitis Both hepatitis B and hepatitis C carry risks in surgery as they are blood-borne pathogens that can be transmitted both from - the patient to the surgeon and vice versa . The usual mode of transmission is blood-to-blood contact through a needle-stick injury or a cut. Many cases of  hepatitis B are asymptomatic and a surgeon may carry the virus without being aware of  it. As - there is an e ff ective vaccine against hepatitis B, surgeons should know their immune status to hepatitis B and be vaccinated against it. Hepatitis C infection often becomes chronic with the risk of  significant liver damage but is potentially curable with interferon-alpha and ribavirin treatment, so surgeons who are exposed to an infection risk should seek medical advice and antibody measurement. Human immunodeficiency virus The type I human immunodeficiency virus (HIV) is one of  the viruses of  surgical importance because it can be transmitted ). by body fluids, particularly blood. It is a retrovirus that has become increasingly prevalent through sexual transmission (both homo- and heterosexual), intravenous drug addiction and in infected blood products used to treat patients with haemophilia in particular. The risk in surgery is mostly through needle-stick injury during operations. The risk of  opportunistic infections (such as Pneumocystis carinii pneumonia, tuberculosis and cytomegalovirus) and neo - plasms (such as Kaposi’s sarcoma and lymphoma) is thereby increased. In the early weeks after HIV infection, there may be a flu like illness and, during the phase of  seroconversion, patients present the greatest risk of  HIV transmission. It is during these early phases that drug treatment, highly active antiretro therapy (HAART), is most e ff ective through the ability of  these drugs to inhibit reverse transcriptase and protease synthesis, which are the principal mechanisms through which HIV can progress. These drugs suppress the virus but do not clear it completely from the body and treated patients can still transmit the virus to others. Within 2 years, untreated HIV can progress to acquired immunodeficiency syndrome (AIDS) in 25–35% of  patients. Universal precautions Patients may present to surgeons for operative treatment if  they have a surgical disease and they are known to be infected or ‘at risk’, or because they need surgical intervention related to their illness for vascular access or a biopsy when they are known to have hepatitis, HIV infection or AIDS. Particular care should be taken when there is a risk of  splashing/aerosol formation, particularly with power tools. Universal precautions have been drawn up by CDC in the USA and largely adopted by the NHS in the UK. In summary , these are: /uni25CF use of  a full face mask ideally , or protective spectacles; /uni25CF use of  fully waterproof, disposable gowns and drapes, par ticularly during seroconversion; /uni25CF boots to be worn, not clogs, to avoid injury from dropped sharps; /uni25CF double gloving needed (a larger size on the inside is more comfortable); /uni25CF allow only essential personnel in theatre; /uni25CF avoid unnecessary movement in theatre; /uni25CF respect is required for sharps, with passage in a kidney dish; /uni25CF slow meticulous operative technique is needed with mini mised bleeding. After contamination Needle-stick injuries are commonest on the non-dominant index finger during operative surgery . Hollow needle injury carries the greatest risk of  viral transmission. The injured part should be washed under running water and the incident reported. Local policies dictate whether postexposure anti *Data from: COVID-19 dashboard by the Center for Systems Science and Engineering (CSSE) at Johns Hopkins University (accessed 16 August 2021). Figure 5.12 (a) (b) retroviral treatment should be given. Occupational health - advice is required after high-risk exposure, together with the need for hepatitis/HIV testing and the option for continuation in a non-operative specialty . viral COVID-19 pandemic The global pandemic of  coronavirus disease 2019 (COVID - 19) was announced by the World Health Organization on 11 March 2020. As of  16 August 2021, more than 207 million cases and more than 4.36 million deaths had been reported in 210 countries.* The rapid spread of  the outbreak has had short-term implications f or global healthcare systems, including the field of  surgery . Many hospitals were forced to stop or postpone elective surgical interventions during the first wave in early to mid-2020. However, emergency surgery and time-sensitive surgery , i.e. cancer surgery , continued with relevant precautions, including the use of  personal protective equipment. COVID-19 is a contagious respiratory and vascular dis - ease. The aetiology is severe acute respiratory syndrome coro - navirus 2 (SARS-CoV-2) ( Figure 5.12a ) , which is a specific type of  coronavirus. Common symptoms include fever, cough, fatigue, shortness of  breath or breathing di ffi culties as well as loss of  smell and taste . The incubation period may range from 1 to 14 days. While most people have mild symptoms, some - people develop acute respiratory distress syndrome (ARDS), possibly precipitated by a cytokine storm; multiorgan failure; septic shock; and hypercoagulable states. Longer term damage to organs (in particular, the lungs and heart) has been observed. Complications in postoperative surgical patients infected with COVID-19 in either an elective or emergency setting may include pneumonia ( Figure 5.12b ) , ARDS, multiorgan failure, se ptic shock and death. Measures to control COVID-19 - related morbidity and mortality have thus been implemented - by many countries, including a mandatory preopera tive cocooning of  elective surgical patients 10–14 days prior to sur - gery and preopera tive COVID-19 swab testing 2–3 days prior to elective surgery . Like many other viral infections, there is no definite pharmacological cure for this infection, although there has been some evidence for supportive care, e .g. with hydroxy - chloroquine and dexamethasone. Multiple vaccines were made available at the end of 2020 and, currently , the majority - of  countries have most of  their population vaccinated. 

Severe acute
respiratory syndrome coronavirus 2
(SARS-CoV-2).
Chest radiograph
showing coronavirus disease 2019
(COVID-19) pneumonia changes.

Viral infections relevant to surgery

Hepatitis Both hepatitis B and hepatitis C carry risks in surgery as they are blood-borne pathogens that can be transmitted both from - the patient to the surgeon and vice versa . The usual mode of transmission is blood-to-blood contact through a needle-stick injury or a cut. Many cases of  hepatitis B are asymptomatic and a surgeon may carry the virus without being aware of  it. As - there is an e ff ective vaccine against hepatitis B, surgeons should know their immune status to hepatitis B and be vaccinated against it. Hepatitis C infection often becomes chronic with the risk of  significant liver damage but is potentially curable with interferon-alpha and ribavirin treatment, so surgeons who are exposed to an infection risk should seek medical advice and antibody measurement. Human immunodeficiency virus The type I human immunodeficiency virus (HIV) is one of  the viruses of  surgical importance because it can be transmitted ). by body fluids, particularly blood. It is a retrovirus that has become increasingly prevalent through sexual transmission (both homo- and heterosexual), intravenous drug addiction and in infected blood products used to treat patients with haemophilia in particular. The risk in surgery is mostly through needle-stick injury during operations. The risk of  opportunistic infections (such as Pneumocystis carinii pneumonia, tuberculosis and cytomegalovirus) and neo - plasms (such as Kaposi’s sarcoma and lymphoma) is thereby increased. In the early weeks after HIV infection, there may be a flu like illness and, during the phase of  seroconversion, patients present the greatest risk of  HIV transmission. It is during these early phases that drug treatment, highly active antiretro therapy (HAART), is most e ff ective through the ability of  these drugs to inhibit reverse transcriptase and protease synthesis, which are the principal mechanisms through which HIV can progress. These drugs suppress the virus but do not clear it completely from the body and treated patients can still transmit the virus to others. Within 2 years, untreated HIV can progress to acquired immunodeficiency syndrome (AIDS) in 25–35% of  patients. Universal precautions Patients may present to surgeons for operative treatment if  they have a surgical disease and they are known to be infected or ‘at risk’, or because they need surgical intervention related to their illness for vascular access or a biopsy when they are known to have hepatitis, HIV infection or AIDS. Particular care should be taken when there is a risk of  splashing/aerosol formation, particularly with power tools. Universal precautions have been drawn up by CDC in the USA and largely adopted by the NHS in the UK. In summary , these are: /uni25CF use of  a full face mask ideally , or protective spectacles; /uni25CF use of  fully waterproof, disposable gowns and drapes, par ticularly during seroconversion; /uni25CF boots to be worn, not clogs, to avoid injury from dropped sharps; /uni25CF double gloving needed (a larger size on the inside is more comfortable); /uni25CF allow only essential personnel in theatre; /uni25CF avoid unnecessary movement in theatre; /uni25CF respect is required for sharps, with passage in a kidney dish; /uni25CF slow meticulous operative technique is needed with mini mised bleeding. After contamination Needle-stick injuries are commonest on the non-dominant index finger during operative surgery . Hollow needle injury carries the greatest risk of  viral transmission. The injured part should be washed under running water and the incident reported. Local policies dictate whether postexposure anti *Data from: COVID-19 dashboard by the Center for Systems Science and Engineering (CSSE) at Johns Hopkins University (accessed 16 August 2021). Figure 5.12 (a) (b) retroviral treatment should be given. Occupational health - advice is required after high-risk exposure, together with the need for hepatitis/HIV testing and the option for continuation in a non-operative specialty . viral COVID-19 pandemic The global pandemic of  coronavirus disease 2019 (COVID - 19) was announced by the World Health Organization on 11 March 2020. As of  16 August 2021, more than 207 million cases and more than 4.36 million deaths had been reported in 210 countries.* The rapid spread of  the outbreak has had short-term implications f or global healthcare systems, including the field of  surgery . Many hospitals were forced to stop or postpone elective surgical interventions during the first wave in early to mid-2020. However, emergency surgery and time-sensitive surgery , i.e. cancer surgery , continued with relevant precautions, including the use of  personal protective equipment. COVID-19 is a contagious respiratory and vascular dis - ease. The aetiology is severe acute respiratory syndrome coro - navirus 2 (SARS-CoV-2) ( Figure 5.12a ) , which is a specific type of  coronavirus. Common symptoms include fever, cough, fatigue, shortness of  breath or breathing di ffi culties as well as loss of  smell and taste . The incubation period may range from 1 to 14 days. While most people have mild symptoms, some - people develop acute respiratory distress syndrome (ARDS), possibly precipitated by a cytokine storm; multiorgan failure; septic shock; and hypercoagulable states. Longer term damage to organs (in particular, the lungs and heart) has been observed. Complications in postoperative surgical patients infected with COVID-19 in either an elective or emergency setting may include pneumonia ( Figure 5.12b ) , ARDS, multiorgan failure, se ptic shock and death. Measures to control COVID-19 - related morbidity and mortality have thus been implemented - by many countries, including a mandatory preopera tive cocooning of  elective surgical patients 10–14 days prior to sur - gery and preopera tive COVID-19 swab testing 2–3 days prior to elective surgery . Like many other viral infections, there is no definite pharmacological cure for this infection, although there has been some evidence for supportive care, e .g. with hydroxy - chloroquine and dexamethasone. Multiple vaccines were made available at the end of 2020 and, currently , the majority - of  countries have most of  their population vaccinated. 

Severe acute
respiratory syndrome coronavirus 2
(SARS-CoV-2).
Chest radiograph
showing coronavirus disease 2019
(COVID-19) pneumonia changes.

# prophylaxis of surgical infection

prophylaxis of surgical infection

Antimicrobials may be produced by living organisms (anti - - biotics) or by synthetic methods. Some are bactericidal, e.g. penicillins and aminoglycosides, and others are bacteriostatic, e.g. tetracycline and erythromycin. In general, penicillins act upon the bacterial cell wall and are most e ff ective against bacteria tha t are multiplying and synthesising new cell wall materials. The aminoglycosides act at the ribosomal level, preventing or distorting the production of proteins required to maintain the integrity of  the enzymes in the bacterial cell. Hospital and formulary guidelines should be consulted for doses and monitoring of  antibiotic therapy . Penicillin Benzylpenicillin has proved most e ff ective against Gram- positive pathogens, including most streptococci, the clostridia and some of  the staphylococci that do not produce β -lactamase. It is still e ff ective against Actinomyces, which is a rare cause of chronic wound infection. It may be used specifically to treat spreading streptococcal infections. Penicillin is valuable even if  other antibiotics are required as part of  multiple therapy for a mixed infection. Some serious infections, e.g. gas gangrene, - require high-dose intravenous benzylpenicillin. Flucloxacillin Flucloxacillin is resistant to β -lactamases, and is therefore of use in treating infections with penicillinase-producing staph - - ylococci that are resistant to benzylpenicillin, but it has poor activity against other pathogens. It has good tissue penetration - and therefore is useful in treating soft-tissue infections and osteomyelitis. - Ampicillin, amoxicillin and co-amoxiclav e Ampicillin and amoxicillin are β -lactam penicillins and can be taken orally or may be given parenterally . Both are e ff ec - tive against Enterobacteriaceae, Enterococcus faecalis and the majority of group D streptococci, but not species of Klebsiella or Pseudomonas. Clavulanic acid has no antibacterial activity itself, but it does inactivate β -lactamases, so can be used in - conjunction with amoxicillin. The combination is known as co-amoxiclav and is useful against β -lactamase-producing bacteria that are resistant to amoxicillin on its own. These include resistant strains of Staphylococcus aureus, Escherichia coli, Haemophilus influenzae, Bacteroides and Klebsiella. - Piperacillin and ticarcillin These are ureidopenicillins with a broad spectrum of  activity against a broad range of  Gram-positive, Gram-negative and anaerobic bacteria. Both are used in combination with β -lactamase inhibitors (tazobactam with piperacillin and clavulanic acid with ticarcillin). They are not active against - MRSA but are used in the treatment of  septicaemia, hospital- acquired pneumonia and complex urinary tract infections, where they are active against Pseudomonas and Proteus spp. and have a synergistic e ff ect when used with aminoglycosides such as gentamicin. There are several β -lactamase-susceptible cephalosporins that are of  value in surgical practice: cefuroxime, cefotaxime and ceftazidime are widely used. The first two are most e ff ective in intra-abdominal skin and soft-tissue infections, being active against Staphylococcus aureus and most Enterobacteriaceae. As a group, the enterococci ( Streptococcus faecalis ) are not sensitive to the cephalosporins. Ceftazidime, although active against the Gram-negative organisms and Staphylococcus aureus e ff ective against Pseudomonas aeruginosa . These cephalosporins may be combined with an aminoglycoside, such as gentamicin, if Gram-negative cover is needed, and an imidazole, such as metronidazole, if  anaerobic cover is needed. Aminoglycosides Gentamicin and tobramycin have similar activity and are e ff ec tive against Gram-negative Enterobacteriaceae. Gentamicin is e ff ective against many strains of Pseudomonas , although resis tance has been recognised. All aminoglycosides are inactive against anaerobes and streptococci. Serum levels immediately before and 1 hour after intramuscular injection must be taken and repeated at 48 hours after the start of  therapy , and dosage should be modified to satisfy peak and trough levels. Ototox icity and nephrotoxicity may follow sustained high toxic levels and therefore single, large doses may be safer. Vancomycin and teicoplanin These glycopeptide antibiotics are most active against Gram-positive aerobic and anaerobic bacteria and have proved to be e ff ective against MRSA, so are often used as prophylactic antibiotics when there is a high risk of  MRSA. They are ototoxic and nephrotoxic, so serum levels should be monitored. They are e ff ective against C. di ff . in cases of pseudomembranous colitis. Meropenem, ertapenem and imipenem are members of  the carbapenems. They are stable to β -lactamase, have useful broad-spectrum anaerobic as well as Gram-positive activity and are e ff ective for the treatment of  resistant organisms, such as ESBL-resistant urinary tract infections or serious mixed-spectrum abdominal infections (peritonitis). Metronidazole , is also Metronidazole is the most widely used member of  the imid - azole group and is active against all anaerobic bacteria. It is particularly safe and may be administered orally , rectally or intravenously . Infections caused by anaerobic cocci and strains of Bacteroides and Clostridia can be treated, or prevented, by its use. Metronidazole is useful for the prophylaxis and treatment - of  anaerobic infections after abdominal, colorectal and pelvic surgery and in the treatment of C. di ff . pseudomembranous - colitis. Ciprofloxacin Quinolones, such as ciprofloxacin, have a broad spectrum of activity against both Gram-positive and Gram-negative bacte - - ria but are particularly useful against Pseudomonas infections. Many UK and European hospitals have restricted their use as a preventive measure against the development of C. di ff . enterocolitis. prophylaxis of surgical infection

Antimicrobials may be produced by living organisms (anti - - biotics) or by synthetic methods. Some are bactericidal, e.g. penicillins and aminoglycosides, and others are bacteriostatic, e.g. tetracycline and erythromycin. In general, penicillins act upon the bacterial cell wall and are most e ff ective against bacteria tha t are multiplying and synthesising new cell wall materials. The aminoglycosides act at the ribosomal level, preventing or distorting the production of proteins required to maintain the integrity of  the enzymes in the bacterial cell. Hospital and formulary guidelines should be consulted for doses and monitoring of  antibiotic therapy . Penicillin Benzylpenicillin has proved most e ff ective against Gram- positive pathogens, including most streptococci, the clostridia and some of  the staphylococci that do not produce β -lactamase. It is still e ff ective against Actinomyces, which is a rare cause of chronic wound infection. It may be used specifically to treat spreading streptococcal infections. Penicillin is valuable even if  other antibiotics are required as part of  multiple therapy for a mixed infection. Some serious infections, e.g. gas gangrene, - require high-dose intravenous benzylpenicillin. Flucloxacillin Flucloxacillin is resistant to β -lactamases, and is therefore of use in treating infections with penicillinase-producing staph - - ylococci that are resistant to benzylpenicillin, but it has poor activity against other pathogens. It has good tissue penetration - and therefore is useful in treating soft-tissue infections and osteomyelitis. - Ampicillin, amoxicillin and co-amoxiclav e Ampicillin and amoxicillin are β -lactam penicillins and can be taken orally or may be given parenterally . Both are e ff ec - tive against Enterobacteriaceae, Enterococcus faecalis and the majority of group D streptococci, but not species of Klebsiella or Pseudomonas. Clavulanic acid has no antibacterial activity itself, but it does inactivate β -lactamases, so can be used in - conjunction with amoxicillin. The combination is known as co-amoxiclav and is useful against β -lactamase-producing bacteria that are resistant to amoxicillin on its own. These include resistant strains of Staphylococcus aureus, Escherichia coli, Haemophilus influenzae, Bacteroides and Klebsiella. - Piperacillin and ticarcillin These are ureidopenicillins with a broad spectrum of  activity against a broad range of  Gram-positive, Gram-negative and anaerobic bacteria. Both are used in combination with β -lactamase inhibitors (tazobactam with piperacillin and clavulanic acid with ticarcillin). They are not active against - MRSA but are used in the treatment of  septicaemia, hospital- acquired pneumonia and complex urinary tract infections, where they are active against Pseudomonas and Proteus spp. and have a synergistic e ff ect when used with aminoglycosides such as gentamicin. There are several β -lactamase-susceptible cephalosporins that are of  value in surgical practice: cefuroxime, cefotaxime and ceftazidime are widely used. The first two are most e ff ective in intra-abdominal skin and soft-tissue infections, being active against Staphylococcus aureus and most Enterobacteriaceae. As a group, the enterococci ( Streptococcus faecalis ) are not sensitive to the cephalosporins. Ceftazidime, although active against the Gram-negative organisms and Staphylococcus aureus e ff ective against Pseudomonas aeruginosa . These cephalosporins may be combined with an aminoglycoside, such as gentamicin, if Gram-negative cover is needed, and an imidazole, such as metronidazole, if  anaerobic cover is needed. Aminoglycosides Gentamicin and tobramycin have similar activity and are e ff ec tive against Gram-negative Enterobacteriaceae. Gentamicin is e ff ective against many strains of Pseudomonas , although resis tance has been recognised. All aminoglycosides are inactive against anaerobes and streptococci. Serum levels immediately before and 1 hour after intramuscular injection must be taken and repeated at 48 hours after the start of  therapy , and dosage should be modified to satisfy peak and trough levels. Ototox icity and nephrotoxicity may follow sustained high toxic levels and therefore single, large doses may be safer. Vancomycin and teicoplanin These glycopeptide antibiotics are most active against Gram-positive aerobic and anaerobic bacteria and have proved to be e ff ective against MRSA, so are often used as prophylactic antibiotics when there is a high risk of  MRSA. They are ototoxic and nephrotoxic, so serum levels should be monitored. They are e ff ective against C. di ff . in cases of pseudomembranous colitis. Meropenem, ertapenem and imipenem are members of  the carbapenems. They are stable to β -lactamase, have useful broad-spectrum anaerobic as well as Gram-positive activity and are e ff ective for the treatment of  resistant organisms, such as ESBL-resistant urinary tract infections or serious mixed-spectrum abdominal infections (peritonitis). Metronidazole , is also Metronidazole is the most widely used member of  the imid - azole group and is active against all anaerobic bacteria. It is particularly safe and may be administered orally , rectally or intravenously . Infections caused by anaerobic cocci and strains of Bacteroides and Clostridia can be treated, or prevented, by its use. Metronidazole is useful for the prophylaxis and treatment - of  anaerobic infections after abdominal, colorectal and pelvic surgery and in the treatment of C. di ff . pseudomembranous - colitis. Ciprofloxacin Quinolones, such as ciprofloxacin, have a broad spectrum of activity against both Gram-positive and Gram-negative bacte - - ria but are particularly useful against Pseudomonas infections. Many UK and European hospitals have restricted their use as a preventive measure against the development of C. di ff . enterocolitis. prophylaxis of surgical infection

Antimicrobials may be produced by living organisms (anti - - biotics) or by synthetic methods. Some are bactericidal, e.g. penicillins and aminoglycosides, and others are bacteriostatic, e.g. tetracycline and erythromycin. In general, penicillins act upon the bacterial cell wall and are most e ff ective against bacteria tha t are multiplying and synthesising new cell wall materials. The aminoglycosides act at the ribosomal level, preventing or distorting the production of proteins required to maintain the integrity of  the enzymes in the bacterial cell. Hospital and formulary guidelines should be consulted for doses and monitoring of  antibiotic therapy . Penicillin Benzylpenicillin has proved most e ff ective against Gram- positive pathogens, including most streptococci, the clostridia and some of  the staphylococci that do not produce β -lactamase. It is still e ff ective against Actinomyces, which is a rare cause of chronic wound infection. It may be used specifically to treat spreading streptococcal infections. Penicillin is valuable even if  other antibiotics are required as part of  multiple therapy for a mixed infection. Some serious infections, e.g. gas gangrene, - require high-dose intravenous benzylpenicillin. Flucloxacillin Flucloxacillin is resistant to β -lactamases, and is therefore of use in treating infections with penicillinase-producing staph - - ylococci that are resistant to benzylpenicillin, but it has poor activity against other pathogens. It has good tissue penetration - and therefore is useful in treating soft-tissue infections and osteomyelitis. - Ampicillin, amoxicillin and co-amoxiclav e Ampicillin and amoxicillin are β -lactam penicillins and can be taken orally or may be given parenterally . Both are e ff ec - tive against Enterobacteriaceae, Enterococcus faecalis and the majority of group D streptococci, but not species of Klebsiella or Pseudomonas. Clavulanic acid has no antibacterial activity itself, but it does inactivate β -lactamases, so can be used in - conjunction with amoxicillin. The combination is known as co-amoxiclav and is useful against β -lactamase-producing bacteria that are resistant to amoxicillin on its own. These include resistant strains of Staphylococcus aureus, Escherichia coli, Haemophilus influenzae, Bacteroides and Klebsiella. - Piperacillin and ticarcillin These are ureidopenicillins with a broad spectrum of  activity against a broad range of  Gram-positive, Gram-negative and anaerobic bacteria. Both are used in combination with β -lactamase inhibitors (tazobactam with piperacillin and clavulanic acid with ticarcillin). They are not active against - MRSA but are used in the treatment of  septicaemia, hospital- acquired pneumonia and complex urinary tract infections, where they are active against Pseudomonas and Proteus spp. and have a synergistic e ff ect when used with aminoglycosides such as gentamicin. There are several β -lactamase-susceptible cephalosporins that are of  value in surgical practice: cefuroxime, cefotaxime and ceftazidime are widely used. The first two are most e ff ective in intra-abdominal skin and soft-tissue infections, being active against Staphylococcus aureus and most Enterobacteriaceae. As a group, the enterococci ( Streptococcus faecalis ) are not sensitive to the cephalosporins. Ceftazidime, although active against the Gram-negative organisms and Staphylococcus aureus e ff ective against Pseudomonas aeruginosa . These cephalosporins may be combined with an aminoglycoside, such as gentamicin, if Gram-negative cover is needed, and an imidazole, such as metronidazole, if  anaerobic cover is needed. Aminoglycosides Gentamicin and tobramycin have similar activity and are e ff ec tive against Gram-negative Enterobacteriaceae. Gentamicin is e ff ective against many strains of Pseudomonas , although resis tance has been recognised. All aminoglycosides are inactive against anaerobes and streptococci. Serum levels immediately before and 1 hour after intramuscular injection must be taken and repeated at 48 hours after the start of  therapy , and dosage should be modified to satisfy peak and trough levels. Ototox icity and nephrotoxicity may follow sustained high toxic levels and therefore single, large doses may be safer. Vancomycin and teicoplanin These glycopeptide antibiotics are most active against Gram-positive aerobic and anaerobic bacteria and have proved to be e ff ective against MRSA, so are often used as prophylactic antibiotics when there is a high risk of  MRSA. They are ototoxic and nephrotoxic, so serum levels should be monitored. They are e ff ective against C. di ff . in cases of pseudomembranous colitis. Meropenem, ertapenem and imipenem are members of  the carbapenems. They are stable to β -lactamase, have useful broad-spectrum anaerobic as well as Gram-positive activity and are e ff ective for the treatment of  resistant organisms, such as ESBL-resistant urinary tract infections or serious mixed-spectrum abdominal infections (peritonitis). Metronidazole , is also Metronidazole is the most widely used member of  the imid - azole group and is active against all anaerobic bacteria. It is particularly safe and may be administered orally , rectally or intravenously . Infections caused by anaerobic cocci and strains of Bacteroides and Clostridia can be treated, or prevented, by its use. Metronidazole is useful for the prophylaxis and treatment - of  anaerobic infections after abdominal, colorectal and pelvic surgery and in the treatment of C. di ff . pseudomembranous - colitis. Ciprofloxacin Quinolones, such as ciprofloxacin, have a broad spectrum of activity against both Gram-positive and Gram-negative bacte - - ria but are particularly useful against Pseudomonas infections. Many UK and European hospitals have restricted their use as a preventive measure against the development of C. di ff . enterocolitis.